National Cholesterol Educational Program

1. National Cholesterol Educational Program Valerie Stoudemire, Pharm.D. Candidate Tejas Shah Pharm.D. Candidate Dr. Jennifer Williams, Pharm.D. presiding Florida A&M University College of Pharmacy

2. NCEP History The National Cholesterol Education Program (NCEP) was created in 1985 by the National Heart, Lung, and Blood Institute To promote cooperation among practitioners, health professionals, state and local government, and community organizations to inform the public of the importance of knowing their cholesterol level

3. NCEP Principles Educational initiatives and messages are based on firm scientific evidence Use various public and private healthcare organizations to assist in developing and carrying out the campaign

4. NCEP Goals Reduce the prevalence of high blood cholesterol in the U.S. Contribute to the reduction of mortality from coronary heart disease.

5. Health Professionals Objectives Increase awareness of : the risk of high cholesterol in relation to CHD the role of weight control and exercise in managing high cholesterol the importance of proper use of cholesterol-lowering drugs the effectiveness of interdisciplinary collaboration among physicians, nurses, dietitians, and pharmacists to control cholesterol levels

6. Patient and the Public Objectives Increase awareness of : the relationship between high cholesterol levels and CHD the importance of knowing their blood cholesterol levels the importance of seeking professional advice and follow-up to control high blood cholesterol dietary principles for reducing cholesterol levels the importance of adhering to cholesterol lowering regimens

7. Community Objectives Increase activities for blood cholesterol control at the state and community levels Increase awareness and knowledge among students, with respect to blood cholesterol and cardiovascular risk factors Promote increased dissemination of scientifically accurate cholesterol-related information by print and electronic media

8. NCEP Web site The NCEP has a variety of materials and channels to educate professional, patients and the public about the benefits of lowering cholesterol levels. Interactive Web site http://www.nhlbi.nih.gov/chd

9. New Features of NCEP CHD patients are now in another category which sets the goal for LDL values even lower. More attention to HDLs as a CHD risk factor. Emphasis on physical activity and weight loss as components for dietary therapy By Spring 2001 new NCEP updates are expected

10. Progression to Atherosclerosis 1) Diet high in cholesterol and saturated fats leads to high levels of LDLs. 2) When concentration of LDL > number of LDL receptors, LDL removal is hindered by the liver. 3) High LDL levels can then easily enter endothelial cells. 4) Oxidized LDL is produced once LDL is engulfed by endothelial cells. 5) Finally, oxidized LDL leads to the progression of atherosclerosis.

11. Overview of CHD

12. U.S. Cholesterol Statistics 52 million Americans are candidates for NCEP dietary therapy. As many as 25% of the adult population has not had their cholesterol measured, and the majority of patients with CHD are not treated to goal LDL-C levels.

13. Emphasis on risk status as a guide to the type and intensity of lipid lowering therapy Emphasis on HDL, a major risk factor for CHD, in screening Emphasis on physical activity and weight reduction to enhance dietary therapy Emphasis on high-risk postmenopausal women and high-risk elderly who are otherwise healthy as candidates for cholesterol lowering therapy. New Features of ATP II

14. NCEP ATP II: Very High Risk: Those at highest risk for future CHD events because of prior CHD or other atherosclerotic disease. High Risk: Patients without evident CHD who are high risk because of high blood cholesterol, together with multiple other CHD risk factors. Low Risk: Patients with high blood cholesterol levels but are at at low risk due to a lack of CV risk factors. Primary Risk Factors

15. Positive Risk Factors Age (Male > 45; Female > 65 or premature menopause without estrogen therapy) Family History (definite MI or sudden death < 55 years in paternal family, or < 65 years in maternal family) Current cigarette smoking Hypertension (> 140/90 mmHg or antihypertensive therapy) Low HDL (< 35 mg/dL) Diabetes mellitus

16. Negative Risk Factor There�s only One! High HDL-cholesterol (> 60 mg/dL)

17. Non-fasting Total Cholesterol and HDL Screen all adults without CHD > 20 years L-cholesterol (> 60 mg/dL) Measurement method LDL-C = TC - (HDL-C + TG/5) *Equation cannot be used when TG > 400 mg/dL Measurement Recommendations

18. Primary & Secondary Prevention Primary prevention is the management of  elevated LDLs in patients without CHD. Diet Exercise Secondary prevention is the management of  elevated LDL in patients with CHD or other  atherosclerotic diseases. Management same as primary prevention above. Drug therapy

19. Detection and Evaluation Screening

20. Method of Management 1) Non-pharmacological Diet low in saturated fats and cholesterol Regular physical activity 2) Pharmacolgical therapy HMG-CoA reductase inhibitors Nicotinic Acid Bile Acid Resins Fibric Acid Derivatives

21. Choosing Drug vs. Diet Therapy Tb 3 on jones notes bout whether diet or drug

22. Goal of dietary therapy is to decrease the intake of serum cholesterol and increase weight loss in overweight patients. Step 1 diet entails a minor reduction in saturated fats and cholesterol sources. Step 2 diet concentrates the focus on the whole diet to further reduce the intake of saturated fats and cholesterol. *All should occur while maintaining a nutritional diet & healthy body weight. Purpose of Dietary Therapy

23. Non-pharmacological (Step 1 & 2 Diet) Dietary Recommendations

24. Pharmacological Therapy MOA: Inhibits 3-hydroxy-3-methylglutary-coenzme A (HMG-CoA) reductase, the enzyme that catalyzes the rate limiting-step in the biosynthesis of cholesterol. ? LDL catabolism, inhibits LDL synthesis, thus ?�s LDL receptors. Efficacy: TC ? 15-45% LDL ? 20-60% HDL ? 5-12% TG ? 10-37% Indications: ? LDL or Combined hyperlipidemia (? LDL & mildly ? TG)

25. Pharmacological Therapy Generic (Brand) Dose Fluvastatin (Lescol) 20-40 mg qd Pravastatin (Pravachol) 10-40 mg qd Lovastatin (Mevacor) 10-40 mg qd Simvastatin (Zocor) 10-80 mg qd Atorvastatin (Lipitor) 10-80 mg qd Cerivastatin (Baycol) 0.3 mg qd

26. MOA: Appears to suppress synthesis of VLDL, IDL, & LDL in the liver. May ? TG catabolism, ? HDL catabolism Efficacy: TC ? 25% LDL ? 10-25% HDL ? 10-40% TG ? 20-50% Indications: High LDL and/or high TG Combined hyperlipidemia Pharmacological Therapy

27. Pharmacological Therapy Generic (Brand) Dose Niacin I.R. (Niacor; Nicolar) 2-6 g divided tid Niacin S.R. (Nicobid; 1-2 g divided bid Tempules; Slo-Niacin) Niaspan 100-2000 mg qd

28. Pharmacological Therapy MOA: Binds to bile acid in the intestines, interrupting enterohepatic circulation and increasing fecal excretion of the acid: ? LDL receptors Efficacy: LDL ? 20-30% Indications: High LDL�s

29. Generic (Brand) Dose Cholestyramine (Questran) 4 gm bid Colestipol granules (Cholestid) 5 gm powder or 4 gm tab bid Pharmacological Therapy

30. MOA: Not fully understood: ? clearance of VLDL by ? action of lipoprotein lipase. ? VLDL production. Efficacy: LDL + 10% HDL ? 10-25% TG ? 40-55% Indications: ? TG Combined hyperlipidemia (?TG & ?HDL) Pharmacological Therapy

31. Pharmacological Therapy Generic (Brand) Dose Gemfibrozil (Lopid) 600 mg bid Fenofibrate cap (Tricor) 67 mg qd