Hyperlipidemia

Saudi Diploma in Family Medicine Center of Post Graduate Studies in Family Medicine
Presented by: Dr. Zekeriya Aktürk zekeriya.akturk@gmail.com www.aile.net

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Top 10 cause of Death in K.S.A.

Top 10 cause of Death in K.S.A.

30 %

•Cardiovascular diseases (CVD) are the main cause of morbidity and mortality among the Saudi population1 •A significant proportion of hospital admissions is due to CVD, whether acute or chronic or to cardiac procedures including angiograms2

1-Al Balla SR,. J Trop Med Hyg 1993;96:157-62 2-Bamgboye EA, Saudi Med J 1993;13(1):8-13. ] .

Prevalence of dyslipidemia in Saudi Adults •The overall prevalence of hypercholesterolemia TC > 200 mg/ dL: 35.4% . Saudi Med J 2005. 26 (12): 1918-1925 .et al.6%.8 Al-Nozha MM. Metabolic syndrome in Saudi Arabia. •The overall prevalence of hypertriglyceridemia TG > 150 mg/ dL) : 49. •HDL Values in men and women Men <40mg/dL: 74.8 % Women <50mg/dL: 81.

M.Hyperlipidemia Michele Ritter. Argy Resident – February.D. 2007 6 / 29 .

• High-density lipoproteins (HDL) carry fat and cholesterol back to the liver for excretion. • LDL then carries fat and cholesterol to the body’s cells. the chylomicrons release triglycerides and some cholesterol and become low-density lipoproteins (LDL).The story of lipids • Chylomicrons transport fats from the intestinal mucosa to the liver • In the liver. 7 / 29 .

The story of lipids (cont.) • When oxidized LDL cholesterol gets high. which causes atherosclerosis. VLDL. atheroma formation in the walls of arteries occurs. IDL 8 / 29 . • Atherogenic cholesterol → LDL. • HDL cholesterol is able to go and remove cholesterol from the atheroma.

Atherosclerosis 9 / 29 .

Causes of Hyperlipidemia • • • • • Diet Hypothyroidism Nephrotic syndrome Anorexia nervosa Obstructive liver disease • Obesity • Diabetes mellitus • Pregnancy • Obstructive liver disease • Acute heaptitis • Systemic lupus erythematousus • AIDS (protease inhibitors) 10 / 29 .

avocados Corn. Raises HDL Polyunsaturated Saturated Whole milk. coconuts. peanut oil. fish Lowers LDL. cashews. Lowers LDL. chicken skin Most margarines. canola oil. olive oil. partially Raises LDL hydrogenated vegetable oil. butter. and ice cream. egg yolks. vegetable shortening. soybean. deep-fried chips. most commercial baked goods Trans 11 / 29 .Dietary sources of Cholesterol Type of Fat Monounsaturated Main Source Effect on Cholesterol levels Olives. coconut HDL oil . coconut milk. Raises HDL almonds. red Raises both LDL and meat. safflower and cottonseed oil. many fast foods. chocolate. cheese. peanuts and most other nuts.

resulting in elevated levels of LDL at birth and throughout life • High risk for atherosclerosis. coccurs in heterozygous form • Occurs in 1 in 500 individuals • Mutation in LDL receptor. tendon xanthomas (75% of patients). a binding-defective form of apoE (which usually plays important role in catabolism of chylomicron and VLDL) • Increased risk for atherosclerosis. peripheral vascular disease • Tuberous xanthomas. • Familial Combined Hyperlipidemia • Autosomal dominant • Increased secretions of VLDLs • Dysbetalipoproteinemia • Affects 1 in 10. tuberous xanthomas and xanthelasmas of eyes. striae palmaris 12 / 29 .000 • Results in apo E2.Hereditary Causes of Hyperlipidemia • Familial Hypercholesterolemia • Codominant genetic disorder.

Checking lipids • Nonfasting lipid panel • measures HDL and total cholesterol • Fasting lipid panel • Measures HDL. total cholesterol and triglycerides • LDL cholesterol is calculated: – LDL cholesterol = total cholesterol – (HDL + triglycerides/5) 13 / 29 .

14 / 29 . or family history of either elevated cholesteral levels or premature cardiovascular disease. LDL. – If total cholesterol > 200 or HDL <40. diabetes. HDL and triglycerides – Repeat testing every 5 years for acceptable values – United States Preventative Services Task Force – Women aged 45 years and older. then a fasting panel should be obtained – Cholesterol screening should begin at 20 years in patients with a history of multiple cardiovascular risk factors. and men ages 35 years and older undergo screening with a total and HDL cholesterol every 5 years.When to check lipid panel • Two different Recommendations – Adult Treatment Panel (ATP III) of the National Cholesterol Education Program (NCEP) – Beginning at age 20: obtain a fasting (9 to 12 hour) serum lipid profile consisting of total cholesterol.

Goals for Lipids • LDL – < 100 →Optimal – 100-129 → Near optimal – 130-159 → Borderline – 160-189→ High – ≥ 190 → Very High • HDL – < 40 → Low – ≥ 60 → High • Serum Triglycerides – – – – < 150 → normal 150-199 → Borderline 200-499 → High ≥ 500 → Very High • Total Cholesterol – < 200 → Desirable – 200-239 → Borderline – ≥240 → High 15 / 29 .

women ≥ 55) 16 / 29 .Determining Cholesterol Goal (LDL!) • Look at JNC 7 Risk Factors • • • • Cigarette smoking Hypertension (BP ≥140/90 or on anti-hypertensives) Low HDL cholesterol (< 40 mg/dL) Family History of premature coronary heart disease (CHD) (CHD in first-degree male relative <55 or CHD in first-degree female relative < 65) • Age (men ≥ 45.

Determining Goal LDL • CHD and CHD Risk Equivalents: – Peripheral Vascular Disease – Cerebral Vascular Accident – Diabetes Mellitus 17 / 29 .

LDL Goals • 0-1 Risk Factors: • LDL goal is 160 • If LDL ≥ 160: Initiate TLC (therapeutic lifestyle changes) • If LDL ≥ 190: Initiate pharmaceutical treatment • 2 + Risk Factors • LDL goal is 130 • If LDL ≥ 130: Initiate TLC • If LDL ≥ 160: Initiate pharmaceutical treatment • CHD or CHD Risk Equivalent • LDL goal is 100 (or 70) • If LDL ≥ 100: Initiate TLC and pharmaceutical treatment 18 / 29 .

Treatment of Hyperlipidemia • Lifestyle modification – Low-cholesterol diet – Exercise 19 / 29 .

↑HDL (10-20) ↓ Triglyceride (20-50) ↓ LDL ↑ HDL No change in triglycerides Bile Acid sequestrants GI distress. myopathy Fibric Acids Gemfibrozil Fenofibrate Cholestyramine ↓LDL (5-20). decreased absorption of other drugs 20 / 29 .↑ HDL (5-15) ↓ Triglycerides (7-30) ↓ LDL( 14-18). constipation. increased liver enzymes Headache. gallstones. ↑ HDL (1-3) ↓ Triglyceride (2) ↓LDL (15-30). Hyperglycemia. ↑ HDL (15-35) ↓ Triglyceride (20-50) Side Effects Myopathy. GI distress. hepatotoxicity Dyspepsia.Medications for Hyperlipidemia Drug Class HMG CoA reductase inhibitors Cholesterol absorption inhibitor Nicotinic Acid Agents Lovastatin Pravastatin Ezetimibe Effects (% change) ↓LDL (18-55). GI distress Flushing. Hyperuricemia.

21 / 29 .

The patient has no family history of premature CAD. Her BMI is 24. Lipoprotein analysis shows a total cholesterol level of 240 mg/dL. Her blood pressure is 135/85 mm Hg. a triglyceride level of 85 mg/dL and a LDL level is 180 mg/dL. She does not smoke or have diabetes and has been postmenopausal for 3 years. an HDL level of 55 mg/dL.Case # 1 • A 55-year-old woman without symptoms of CAD seeks assessment and advice for routine health maintenance. 22 / 29 .

) • What is the goal LDL in this woman? • What would you do if exercise/diet change do not improve cholesterol after 3 months? • How would your management change if she complained of claudication with walking? 23 / 29 .Case # 1 (cont.

He has no complaints but is worried because his father had a “heart attack” at the age of 45. He is a current smoker and has a 23-pack year history of tobacco use. A fasting lipid panel reveals a LDL 170 mg/dL and an HDL of 35 mg/dL.Case # 2 • A 40. Serum Triglycerides were 140 mg/dL.year-old man without significant past medical history comes in for a routine annual exam. 24 / 29 . Serum chemistries including liver panel are all normal.

what? 25 / 29 .) • What is this patient’s goal LDL? • Would you start medication.Case # 2 (cont. and if so.

26 / 29 . She had a normal exercise stress test last year prior to knee replacement surgery and has never had symptoms of CHD. She has been told her cholesterol was elevated in the past and states that she has been following a “low cholesterol diet” for the past 6 months after seeing a dietician. HDL 30 and a total triglyceride of 300. and hypertension comes to your office for the first time. obesity. A fasting lipid profile was performed and revealed a LDL 130. Her Hgba1c is 6.Case # 3 • A 65 year-old woman with medical history of Type II diabetes.5%.

Case # 3 (cont.) • What is this patient’s goal LDL? • What medication would you consider starting in this patient? • What labs would you want to monitor in this patient? 27 / 29 .

USAF. Reamy. MD. Colonel. MC Chair – Department of Family Medicine Uniformed Services University 28 / 29 .HYPERLIPIDEMIA Brian V.

still our nation’s #1 killer 29 / 29 .Why Bother? • Optimum treatment of lipids helps in the primary & secondary prevention of ASCVD.

• HUGE opportunity to prevent disease!! 30 / 29 .Why Bother? • ASCVD has been #1 cause of death every year since 1900 with exception of 1918. • 50% of CVD diagnoses and 15% of CVD deaths are in patients < 65 years of age • Many young adults have 2 or more risk factors that go unrecognized and untreated.

nih.gov LDL goals lowered Raised acceptable HDL to 40 Lowered TG goal to 150 Risk Factor assessment enhanced with the 10-yr Framingham risk calculator • Added the Metabolic Syndrome to Tx 31 / 29 .NCEP/ATP III – 15 May 2001 • • • • • www.nhlbi.

• Interpret: LDL < 100mg/dl optimal LDL 100-129 near optimal LDL 130-159 borderline high LDL 160-189 high LDL >190 very high (mg/dl x 0.0259mmol/l = SI units) 32 / 29 .NCEP/ATP III – 9 Steps • Step 1: Obtain. complete & fasting lipids.

do Framingham 10-yr risk assessment. AAA. FHx. DM. Age & Sex. Carotid) • Step 3: Risk factor assessment (HTN.NCEP/ATP III • Step 2: Identify if patient has CAD or equivalent (PAD. 33 / 29 . Tob. HDL<40 or >60) • Step 4: If 2 or more risk factors.

Framingham Ten Year Risk Men Women 34 / 29 .

Framingham Ten Year Risk 0 35 / 29 .

Framingham Ten Year Risk 0 3 0 Non-Smoker 36 / 29 .

Framingham Ten Year Risk
0 3 0 1
HDL = 43

37 / 29

Framingham Ten Year Risk
0 3 0 1 0 4
38 / 29

SBP = 119, untreated

Framingham Ten Year Risk
0 3 0 1 0 4
39 / 29

NCEP/ATP III – Step 5
Risk CategoryLDL Goal Start T.L.C. Start Drug Treatment >100mg/dl >100 – 129mg/dl >130 – 160mg/dl >160 – 40 / 29 190mg/dl

CHD/10yr risk>20% (high) 2+RF or 10yr<20% (Medium)

<100mg/dl

<130mg/dl

>130mg/dl

0-1 risk <160mg/dl factors (low)

>160mg/dl

lower LDL 10% – Increased exercise – Weight management 41 / 29 . Take Control® margarines) .NCEP/ATP III – Step 6 • Initiate Therapeutic Lifestyle Changes (TLC) – AHA Step 2 diet – Soluble fiber 10-25gm/day – Plant sterols/Sitostanol (Benecol®.

42 / 29 .1. • Best unbiased source for review of drug treatment: “The Medical Letter: Choice of lipid regulating drugs” 43:2001.pp43-48 and 2003. Add drugs after 3 months if TLC not effective in other risk categories.NCEP/ATP III – Step 7 • Add drug therapy simultaneously to TLC in patients with CHD or equivalent.77-79.

GI side effects/malabsorption issues • Niacin. NIASPAN® easier to tolerate. Caution with Diabetes. colesevelam): lower LDL.(cholestyramine. cheap & moves every parameter in the right direction. Need slow dose titration and pre-med with ASA.colestid. 43 / 29 . Most potent agent at increasing HDL.“miracle agent”.5 at baseline. adjunct to statins. side effects problematic.) • Resins.Drugs – Step 7 (cont. But. can worsen glycemic control if HBA1C >7.

Can combine with statins but caution re: hepatic side effects. *Fenofibrate qd & less side effects.Drugs – Step 7 (cont) • Fibrates – (fenofibrate. gemfibrozil) lower TG and raise HDL. >$$ • If combining w/ a statin use fenofibrate. Cutting statin dose by ½ is good rule. gemfibrozil has > rates of rhabdomyolysis 44 / 29 .

VERY well tolerated at 10mg/d. 45 / 29 . Combined with a statin increases effects of statin by 10-15% w/o side effects. increases HDL by 1.Newer Drugs – Step 7 (cont. Lowers LDL 17%. TG 6%.new class that inhibits the intestinal absorption of cholesterol.3%.) • Ezetimibe (Zetia®).

Causes less flushing and hepatic effects than any niacin formulation. Greater risk of myopathy than a statin alone.Newer Drugs – Step 7 (cont) • Lovastatin + Niacin (Advicor®). 20/1000. 46 / 29 . Increase dose monthly up to max 40/2000.in fixed combos 20/500. and HDL increase by 41%. 20/750. Max dose w/ LDL decrease 45%. TG 42%.

caution in folks on warfarin 47 / 29 .Newer Drugs – Step 7 • Simvastatin(10/20/40/80) + Ezetimibe 10mg: VYTORIN® • OMACOR: concentrated omega-3’s. 4 capsules = 12 OTC fish oil capsules • Can interfere with clotting times.

Drugs – Step 7 (cont.04. . None safe in pregnancy.hepatitis (transaminases>3x nl. (cerivistatin was 16-80x these rates!!) 48 / 29 . incidence rates per million Rx’s: pravastatin0.) = 0.5% .rhabdomyolysis = rare.12.19 atorvastatin 0. simvastatin 0. lovastatin0.) • Statins.muscle pain = 1-5% .04.All w/ anti-inflammatory effects. All are more potent by 10-15% with evening dosing.

potent • Fluvastatin: less potent. 5 . may raise HDL a bit more & lower TG. take on empty stomach • Simvastatin: lots of prevention data. poor prevention data • Rosuvastatin: most potent.40 mg (CRESTOR®).Drugs – Step 7 (cont. generic version • Pravastatin: least drug interactions due to different elimination pathway. Caution w/ CrCl<30cc/min and in Asian subpopulations at higher doses.) • Atorvastatin – great LDL & TG lowering • Lovastatin: take w/ food. 49 / 29 .

are not a reason to stop the statin – they are are a reason to watch closely.Statin Pearls • Elevated transaminases on statins. not always class specific. 50 / 29 . • Unexplained myalgias may occur on statins without CK elevation. (unless reaching 3x normal). Try a different statin. • Statin side effects are often agent specific.

• Unless you enjoy driving yourself nuts.Statin Pearls • Rhabdomyolysis is uncommon unless CK is elevated to 10 x normal. do not check CK serially in patients on statins. • But – what about the PROVE-IT study? (NEJM 8 April 2004) 51 / 29 . Remember vigorous yard work will bump your CK! Some think a baseline CK may be helpful. Usually occurs in patients with multiple co-morbidities.

atorvastatin was superior as early as 30 days of therapy.PROVE-IT Trial • Designed to “PROVE” that 80mg atorvastatin was no better than 40 mg pravastatin in secondary prevention. 28% less mortality than pravastatin group (meanLDL=95) 52 / 29 . • But. In just 24 mths the atorvastatin group (meanLDL=62) had 16% less of all CV events.

53 / 29 .PROVE-IT Trial • WOW! • Evidence from mammalian species had shown that atherogenesis stops & reverses at an LDL <80 – now some clinical outcome data.

PROSPER. HPS. ALLHAT. LDL <100 new goal • Felt that drug treatment should aim for at least a 30-40% LDL reduction. 54 / 29 .NCEP Update 13 July 2004 • Circulation 13 July 2004:227-239 • Added the results of PROVE-IT. ASCOT • Confirmed ATP-III and added that in very high risk an LDL goal <70 was optional • For patients at moderately high risk = 10-20% Framingham risk.

High 10-20% Moderate <10% 10yr LOW LDL <70mg/dl Optional <100mg/dl Optional <130mg/dl <160mg/dl TLC >100mg/dl >130mg/dl >130mg/dl >160mg/dl DRUGS >100mg/dl or <100mg >130mg/dl or 100-130 >160mg/dl >190mg/dl 55 / 29 .Updated ATP-III Guidelines RISK HIGH >20% 10yr Mod.

2 groups for 4.001 patients.9 years with mean LDL = 99mg/dl before study – 10 mg atorvastatin (mean LDL=101mg/dl) – 80 mg atorvastain (mean LDL=77mg/dl) 56 / 29 .TNT Study “Treat to New Targets” • NEJM 7 April 2005: Prospective trial at lowering LDL well below 100mg/dl in adults with CHD (secondary prevention) • 10.

Results • Side Effects: increased LFT’s in 0.2% in major cardiovascular events for group with LDL <80 versus group with LDL=101. • Results: Relative risk reduction of 22% and absolute risk reduction of 2.TNT . • More evidence to lower our LDL goals… 57 / 29 . No change in rhabdomyolysis risk.2% on high dose.2% of patients on low dose and 1.

35”women Aggressively: – Treat underlying causes of overweight and physical inactivity. use ASA for CHD patients 58 / 29 . TG>150.NCEP/ATP III – Step 8 • Identify Metabolic Syndrome: (3 of 5) – SBP>130. HDL<40 in men and <50 in women. FBS>110. waist>40”men. – Treat HTN.

59 / 29 . first lower triglycerides to prevent pancreatitis. When they are <500 then return to LDL lowering – Treat HDL <40 after lowering LDL. if TG still >200 consider adding/increasing drug therapy – But.NCEP/ATP III – Step 9 • Treat elevated TG (>150mg/dl) – First lower LDL. if TG >500mg/dl.

• All present real Family Practice dilemmas.CASES • All real cases. • Use cases to convey cutting edge info. • Will use the evidence to help formulate a “best” answer. No “perfect answers”. 60 / 29 .

Case # 4 – “Middle-of the Road” • 45 year old woman who on a routine lipid screen has the following values: • TC = 203 HDL=48 TG = 155 LDL = 124 • PMHx: negative. M age 64 • PE: 65” 130lbs P=72 BP=118/68 61 / 29 . smoker • Meds: daily vitamin • FHx: MI in F age 60.

Case #4 – “Middle of the Road” • Risk Factors: 2 . • What do you do with this “middle-of-theroad” risk profile? 62 / 29 . concerns remain: FHx. both less than ideal.g. HDL is <50 & TG >150. <130 • But. e. Framingham = 5% risk • NCEP/ATP III says that she is at her LDL goal. Smoking.

63 / 29 . sudden cardiac death. PAD.Case# 4 – Middle of the Road • • • • Consider a new idea: measure her hs-CRP Facts: CRP is a marker of inflammation.CVA. ASCVD is a disease of inflammation Multiple prospective epidemiological (vs. interventional studies) have shown that CRP can predict MI.

consider 1° inflammatory disease. • < 1mg/l = low risk • 1-3mg/l = moderate risk • >3mg/l = high risk • >10mg/l = invalid for cardiac risk prediction. can check non-fasting. anytime of day. trauma. serious infection.Case #4 – Middle of the Road • Hs-CRP assays are now widely available. 64 / 29 .

And other trials have proven that Statins lower CRP 15-25% within 6 weeks of initiation. exercise and smoking cessation also lower CRP. JAMA 2001:286. 65 / 29 .Case #4 – Middle of the Road • PRINCE (PRavastatin INflammation/Crp Evaluation trial.64-70. • Weight loss.

0mg/l (JUPITER). • How to answer this ? • 2003: 15.Case # 4 – Middle of the Road • CARE & AFCAPS/TEXCAPS both suggest that the benefit of statin therapy among those with low LDL but high CRP may be as large as those with overt hyperlipidemia.000 patients with LDL<130 but CRP above 2. What will happen? 66 / 29 . All will be put on CRESTOR® for prevention.

• Review.Case # 4 – Middle of the Road • What does this mean for our patient? • CRP is most useful in those judged at intermediate risk and in primary prevention. 45 yr old woman with an LDL<130 but +FHX and other borderline risks…eg a 5% Framingham risk • HOW about checking an hs-CRP to further assess her risk ? 67 / 29 .

Doctor! 68 / 29 .2mg/l HIGH risk • Studies have proven she is in fact at risk. no prospective proof that this will change her outcome. It is your call. What to do? • Smoking cessation will lower CRP • Statins will lower her CRP • But.Case # 4 – Middle of the Road • CRP = 3. more than her LDL would tell us.

Apo B. LDL particle size Homocysteine Plasma Adiponectin 69 / 29 .Other Novel Risk Factors • • • • EBCT (coronary Ca++ score) Lp (a) lipoprotein.

11-100 = mild disease. 101400 = non-obstructive disease. it is an alternative. 70 / 29 .EBCT/Coronary Ca++ scores • Coronary Ca++ occurs due to ASCVD • Normal score=0-10. >400 = obstructive • Significant false positives and poor data in women and younger patients • It may not provide incremental information above that obtained with conventional risk factor assessment.

• In patients w/ intermediate risk an EBCT score >80 has a sensitivity of 85% and a specificity of 75% for the risk of events. it is not very useful in low risk or very high risk patients. • Best used in intermediate risk folks where it might change treatment approach. 71 / 29 . It significantly correlates w/ cheaper hs-CRP.EBCT • Like with hs-CRP.

“D” recommendation for adults at low risk. “absence of evidence that detection ultimately results in improved health outcomes. and because false positive tests are likely to cause harm…” • “I” recommendation for those at high risk 72 / 29 .EBCT/Coronary Ca++ Scores • USPSTF: Feb 2004.

• Homocysteine may enhance inflammation & thrombosis.Homocysteine • High plasma homocysteine may be directly related to atherosclerosis development. • There may be no causal association between elevated homocysteine and CV disease risk. • New Evidence!! 73 / 29 .

2 studies re: homocysteine lowering • #1: Secondary prevention: 5522 patients: placebo vs 2.Homocysteine • NEJM.” 74 / 29 .5mg Folate+B6+B12: did not reduce the risk of cardiovascular event. • #2: 3749 pts post-MI: “treatment with Bvitamins did not lower risk of recurrent CV disease. 13 April 2006. A harmful effect of B-vitamin Tx was suggested. more pts in Tx had unstable angina.

Lipid Sub-fractions & other markers • Lipoprotein a. Apolipoprotein B. LDL particle size – All have predictive value for CHD. But not widely available. less reproducible and still no outcome studies. 75 / 29 . expensive. indeed LDL particle size is more precise than LDL alone.

mild OA • MEDS: ASA. Metoprolol 50 mg po bid. ED. “follow-up with your family doctor to get your cholesterol in control” • PMHX: HTN x 20 yrs. At his last visit with his CT surgeon he was told.Case # 5 – The Unreachable Goal • 60 yr old male returns to see you 3 months after a 4vCABG. Viagra®. He feels great. Simvastatin 20 mg po qd • FHX: F with CVA at 68 76 / 29 . BPH.

healed median sternotomy scar • Ext: no edema Lungs: slight dec. no jvd. breath sounds • TC=180.Case # 5 – The Unreachable Goal • PE: 70” 160lbs P=60 BP=124/76 • Cor: RRR. no m/r/g. HDL=42 TG=100 LDL=118 77 / 29 .

2° prev. 78 / 29 .Case # 5 – The Unreachable Goal • Risk Assessment = he has CHD. Also the PROVEIT trial shows that an LDL of 62 was superior to an LDL of 95. • Goal LDL is <100 per ATP III (<70-80 TNT trial data and ATP update) • At this level atherogenesis seems to arrest • At an LDL of 80 in mammalian species atherogenesis reverses.

Case #5 – The Unreachable Goal • You decide to increase the simvastatin to 40mg po qd. TC= 170 TG=105 HDL=42 LDL=107 • What do you do? 79 / 29 . • 6 weeks later.

A threefold higher dose by 12% and a fourfold increase lowers LDL cholesterol by only 18%.Case # 5 – The Unreachable Goal • Many options: 1)increase simvastatin to 80 mg or change to atorvastatin or rosuvastatin. 80 / 29 . • PROBLEM: inc risk of side effects and less LDL lowering effect as you inc statin doses. LDL decreases by only 6 %. For every doubling of dose.

) Be satisfied and await more trials… 81 / 29 . add soluble fiber. add omega-3 fatty acids.Case # 5 – The Unreachable Goal • 2.) Add Ezetimibe 10 mg po qd: less chance of side effects. • 4.) Intensify diet. Ornish Plan. should help to reach goal LDL easily. add soy. • 3.

gov is useful.nih.nhlbi. 3) The key step is risk assessment & then tailoring treatment to individual risk.Summary • 8 Points to make you strong • 1) 1° & 2° prevention of ASCVD are possible! 2) NCEP/ATP III at www. 82 / 29 .

Summary – 8 Points • 3) Better medication options are a help: Ezetimibe. new statins and a cleaner understanding of statin side effects • 4)Attack the metabolic syndrome!! A multi-modal treatment plan is best. 83 / 29 . Advicor®. • 5) Don’t ignore a chance for prevention because your patient is >70 or <35.

Summary – 8 Points • 6) hs-CRP is a powerful new tool to predict risk. 7) Try to get to goal. 84 / 29 . especially in those at intermediate risk. we need prospective proof that lowering it will help reduce ASCVD endpoints. anticipate new ATPIV guidelines. But.

Thanks for your Attention! 85 / 29 .

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