Hyperlipidemia

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Hyperlipidemia
Saudi Diploma in Family Medicine Center of Post
Graduate Studies in Family Medicine
Presented by Dr. Zekeriya Aktürk zekeriya.akturk_at_
gmail.com www.aile.net
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Top 10 cause of Death in K.S.A.
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Top 10 cause of Death in K.S.A.
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• 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 199396157-62

2-Bamgboye EA, Saudi Med J 199313(1)8-13. .
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Prevalence of dyslipidemia in Saudi Adults

• The overall prevalence of hypercholesterolemia
• TC gt 200 mg/ dL 35.4 .
• The overall prevalence of hypertriglyceridemia
• TG gt 150 mg/ dL) 49.6.
• HDL Values in men and women
• Men lt40mg/dL 74.8
• Women lt50mg/dL 81.8

Al-Nozha MM.et al. Metabolic syndrome in Saudi
Arabia. Saudi Med J 2005 26 (12) 1918-1925
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Hyperlipidemia

• Michele Ritter, M.D.
• Argy Resident February, 2007

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The story of lipids

• Chylomicrons transport fats from the intestinal
  mucosa to the liver
• In the liver, the chylomicrons release
  triglycerides and some cholesterol and become
  low-density lipoproteins (LDL).
• LDL then carries fat and cholesterol to the
  bodys cells.
• High-density lipoproteins (HDL) carry fat and
  cholesterol back to the liver for excretion.

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The story of lipids (cont.)

• When oxidized LDL cholesterol gets high, atheroma
  formation in the walls of arteries occurs, which
  causes atherosclerosis.
• HDL cholesterol is able to go and remove
  cholesterol from the atheroma.
• Atherogenic cholesterol ? LDL, VLDL, IDL

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Atherosclerosis
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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)

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

• Familial Hypercholesterolemia
• Codominant genetic disorder, coccurs in
  heterozygous form
• Occurs in 1 in 500 individuals
• Mutation in LDL receptor, resulting in elevated
  levels of LDL at birth and throughout life
• High risk for atherosclerosis, tendon xanthomas
  (75 of patients), tuberous xanthomas and
  xanthelasmas of eyes.
• Familial Combined Hyperlipidemia
• Autosomal dominant
• Increased secretions of VLDLs
• Dysbetalipoproteinemia
• Affects 1 in 10,000
• Results in apo E2, 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, striae palmaris

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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)

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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, LDL, HDL and triglycerides
• Repeat testing every 5 years for acceptable
  values
• United States Preventative Services Task Force
• Women aged 45 years and older, and men ages 35
  years and older undergo screening with a total
  and HDL cholesterol every 5 years.
• If total cholesterol gt 200 or HDL lt40, then a
  fasting panel should be obtained
• Cholesterol screening should begin at 20 years in
  patients with a history of multiple
  cardiovascular risk factors, diabetes, or family
  history of either elevated cholesteral levels or
  premature cardiovascular disease.

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Goals for Lipids

• LDL
• lt 100 ?Optimal
• 100-129 ? Near optimal
• 130-159 ? Borderline
• 160-189? High
• 190 ? Very High
• Total Cholesterol
• lt 200 ? Desirable
• 200-239 ? Borderline
• 240 ? High

• HDL
• lt 40 ? Low
• 60 ? High
• Serum Triglycerides
• lt 150 ? normal
• 150-199 ? Borderline
• 200-499 ? High
• 500 ? Very High

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Determining Cholesterol Goal(LDL!)

• Look at JNC 7 Risk Factors
• Cigarette smoking
• Hypertension (BP 140/90 or on anti-hypertensives)
  
• Low HDL cholesterol (lt 40 mg/dL)
• Family History of premature coronary heart
  disease (CHD) (CHD in first-degree male relative
  lt55 or CHD in first-degree female relative lt 65)
• Age (men 45, women 55)

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Determining Goal LDL

• CHD and CHD Risk Equivalents
• Peripheral Vascular Disease
• Cerebral Vascular Accident
• Diabetes Mellitus

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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

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Treatment of Hyperlipidemia

• Lifestyle modification
• Low-cholesterol diet
• Exercise

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

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

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Case 1 (cont.)

• 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?

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Case 2

• A 40- year-old man without significant past
  medical history comes in for a routine annual
  exam. 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. Serum Triglycerides were 140 mg/dL.
  Serum chemistries including liver panel are all
  normal.

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Case 2 (cont.)

• What is this patients goal LDL?
• Would you start medication, and if so, what?

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Case 3

• A 65 year-old woman with medical history of Type
  II diabetes, obesity, and hypertension comes to
  your office for the first time. 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. She had a normal exercise
  stress test last year prior to knee replacement
  surgery and has never had symptoms of CHD. A
  fasting lipid profile was performed and revealed
  a LDL 130, HDL 30 and a total triglyceride of
  300. Her Hgba1c is 6.5.

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Case 3 (cont.)

• What is this patients goal LDL?
• What medication would you consider starting in
  this patient?
• What labs would you want to monitor in this
  patient?

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HYPERLIPIDEMIA

• Brian V. Reamy, MD, Colonel, USAF, MC
• Chair Department of Family Medicine
• Uniformed Services University

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Why Bother?

• Optimum treatment of lipids helps in the primary
  secondary prevention of ASCVD still our
  nations 1 killer

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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 lt 65 years of age
• Many young adults have 2 or more risk factors
  that go unrecognized and untreated.
• HUGE opportunity to prevent disease!!

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NCEP/ATP III 15 May 2001

• www.nhlbi.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

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NCEP/ATP III 9 Steps

• Step 1 Obtain, complete fasting lipids.
• Interpret LDL lt 100mg/dl optimal
• LDL 100-129 near optimal
• LDL 130-159 borderline high
• LDL 160-189 high
• LDL gt190 very high
• (mg/dl x 0.0259mmol/l SI units)
  

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NCEP/ATP III

• Step 2 Identify if patient has CAD or equivalent
  (PAD, DM, AAA, Carotid)
• Step 3 Risk factor assessment (HTN, FHx, Tob,
  Age Sex, HDLlt40 or gt60)
• Step 4 If 2 or more risk factors do Framingham
  10-yr risk assessment.

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Framingham Ten Year Risk
Men
Women
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Framingham Ten Year Risk
0
36
Framingham Ten Year Risk
0
3
Non-Smoker
0
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Framingham Ten Year Risk
0
3
HDL 43
0
1
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Framingham Ten Year Risk
0
3
0
SBP 119, untreated
1
0 4
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Framingham Ten Year Risk
0
3
0
1
0 4
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NCEP/ATP III Step 5
Risk Category LDL Goal Start T.L.C. Start Drug Treatment
CHD/10yr riskgt20 (high) lt100mg/dl gt100mg/dl gt100 129mg/dl
2RF or 10yrlt20 (Medium) lt130mg/dl gt130mg/dl gt130 160mg/dl
0-1 risk factors (low) lt160mg/dl gt160mg/dl gt160 190mg/dl
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NCEP/ATP III Step 6

• Initiate Therapeutic Lifestyle Changes (TLC)
• AHA Step 2 diet
• Soluble fiber 10-25gm/day
• Plant sterols/Sitostanol (Benecol, Take Control
  margarines) - lower LDL 10
• Increased exercise
• Weight management

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NCEP/ATP III Step 7

• Add drug therapy simultaneously to TLC in
  patients with CHD or equivalent. Add drugs after
  3 months if TLC not effective in other risk
  categories.
• Best unbiased source for review of drug
  treatment The Medical Letter Choice of lipid
  regulating drugs 432001,pp43-48 and
  2003177-79.

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Drugs Step 7 (cont.)

• Resins- (cholestyramine,colestid, colesevelam)
  lower LDL adjunct to statins GI side
  effects/malabsorption issues
• Niacin- miracle agent, cheap moves every
  parameter in the right direction. But, side
  effects problematic. NIASPAN easier to
  tolerate. Need slow dose titration and pre-med
  with ASA. Caution with Diabetes can worsen
  glycemic control if HBA1C gt7.5 at baseline. Most
  potent agent at increasing HDL.

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Drugs Step 7 (cont)

• Fibrates (fenofibrate, gemfibrozil) lower TG
  and raise HDL. Can combine with statins but
  caution re hepatic side effects. Cutting statin
  dose by ½ is good rule. Fenofibrate qd less
  side effects, gt
• If combining w/ a statin use fenofibrate
  gemfibrozil has gt rates of rhabdomyolysis

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Newer Drugs Step 7 (cont.)

• Ezetimibe (Zetia)- new class that inhibits the
  intestinal absorption of cholesterol. Lowers LDL
  17, TG 6, increases HDL by 1.3. Combined with
  a statin increases effects of statin by 10-15
  w/o side effects. VERY well tolerated at 10mg/d.
  

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Newer Drugs Step 7 (cont)

• Lovastatin Niacin (Advicor)- in fixed combos
  20/500, 20/750, 20/1000. Increase dose monthly up
  to max 40/2000. Max dose w/ LDL decrease 45, TG
  42, and HDL increase by 41. Causes less
  flushing and hepatic effects than any niacin
  formulation. Greater risk of myopathy than a
  statin alone.

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Newer Drugs Step 7

• Simvastatin(10/20/40/80) Ezetimibe 10mg
  VYTORIN
• OMACOR concentrated omega-3s 4 capsules 12
  OTC fish oil capsules
• Can interfere with clotting times caution in
  folks on warfarin

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Drugs Step 7 (cont.)

• Statins- All w/ anti-inflammatory effects. None
  safe in pregnancy. All are more potent by 10-15
  with evening dosing.
• - muscle pain 1-5
• - hepatitis (transaminasesgt3x nl.) 0.5
• - rhabdomyolysis rare incidence rates per
  million Rxs pravastatin0.04, lovastatin0.19
• atorvastatin 0.04, simvastatin 0.12.
• (cerivistatin was 16-80x these
  rates!!)

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Drugs Step 7 (cont.)

• Atorvastatin great LDL TG lowering
• Lovastatin take w/ food generic version
• Pravastatin least drug interactions due to
  different elimination pathway take on empty
  stomach
• Simvastatin lots of prevention data, potent
• Fluvastatin less potent poor prevention data
• Rosuvastatin most potent 5 - 40 mg (CRESTOR)
  may raise HDL a bit more lower TG. Caution w/
  CrCllt30cc/min and in Asian subpopulations at
  higher doses.

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Statin Pearls

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

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Statin Pearls

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

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PROVE-IT Trial

• Designed to PROVE that 80mg atorvastatin was no
  better than 40 mg pravastatin in secondary
  prevention.
• But, atorvastatin was superior as early as 30
  days of therapy. In just 24 mths the
  atorvastatin group (meanLDL62) had 16 less of
  all CV events. 28 less mortality than
  pravastatin group (meanLDL95)

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PROVE-IT Trial

• WOW!
• Evidence from mammalian species had shown that
  atherogenesis stops reverses at an LDL lt80
  now some clinical outcome data.

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NCEP Update 13 July 2004

• Circulation 13 July 2004227-239
• Added the results of PROVE-IT, HPS, PROSPER,
  ALLHAT, ASCOT
• Confirmed ATP-III and added that in very high
  risk an LDL goal lt70 was optional
• For patients at moderately high risk 10-20
  Framingham risk LDL lt100 new goal
• Felt that drug treatment should aim for at least
  a 30-40 LDL reduction.

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Updated ATP-III Guidelines
RISK LDL TLC DRUGS
HIGH gt20 10yr lt70mg/dl Optional gt100mg/dl gt100mg/dl or lt100mg
Mod. High 10-20 lt100mg/dl Optional gt130mg/dl gt130mg/dl or 100-130
Moderate lt10 10yr lt130mg/dl gt130mg/dl gt160mg/dl
LOW lt160mg/dl gt160mg/dl gt190mg/dl
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TNT StudyTreat to New Targets

• NEJM 7 April 2005 Prospective trial at lowering
  LDL well below 100mg/dl in adults with CHD
  (secondary prevention)
• 10,001 patients 2 groups for 4.9 years with mean
  LDL 99mg/dl before study
• 10 mg atorvastatin (mean LDL101mg/dl)
• 80 mg atorvastain (mean LDL77mg/dl)

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TNT - Results

• Side Effects increased LFTs in 0.2 of patients
  on low dose and 1.2 on high dose. No change in
  rhabdomyolysis risk.
• Results Relative risk reduction of 22 and
  absolute risk reduction of 2.2 in major
  cardiovascular events for group with LDL lt80
  versus group with LDL101.
• More evidence to lower our LDL goals

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NCEP/ATP III Step 8

• Identify Metabolic Syndrome (3 of 5)
• SBPgt130, FBSgt110, TGgt150, HDLlt40 in men and lt50
  in women, waistgt40men, 35women
• Aggressively
• Treat underlying causes of overweight and
  physical inactivity.
• Treat HTN, use ASA for CHD patients

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NCEP/ATP III Step 9

• Treat elevated TG (gt150mg/dl)
• First lower LDL if TG still gt200 consider
  adding/increasing drug therapy
• But, if TG gt500mg/dl, first lower triglycerides
  to prevent pancreatitis. When they are lt500 then
  return to LDL lowering
• Treat HDL lt40 after lowering LDL.

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CASES

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

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Case 4 Middle-of the Road

• 45 year old woman who on a routine lipid screen
  has the following values
• TC 203 HDL48 TG 155 LDL 124
• PMHx negative, smoker
• Meds daily vitamin
• FHx MI in F age 60, M age 64
• PE 65 130lbs P72 BP118/68

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Case 4 Middle of the Road

• Risk Factors 2 Framingham 5 risk
• NCEP/ATP III says that she is at her LDL goal
  e.g. lt130
• But, concerns remain FHx, Smoking, HDL is lt50
  TG gt150 both less than ideal.
• What do you do with this middle-of-the-road
  risk profile?

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Case 4 Middle of the Road

• Consider a new idea measure her hs-CRP
• Facts CRP is a marker of inflammation.
• ASCVD is a disease of inflammation
• Multiple prospective epidemiological (vs.
  interventional studies) have shown that CRP can
  predict MI,CVA, PAD, sudden cardiac death.

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Case 4 Middle of the Road

• Hs-CRP assays are now widely available can check
  non-fasting, anytime of day.
• lt 1mg/l low risk
• 1-3mg/l moderate risk
• gt3mg/l high risk
• gt10mg/l invalid for cardiac risk
  predictionconsider 1 inflammatory disease,
  trauma, serious infection.

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Case 4 Middle of the Road

• PRINCE (PRavastatin INflammation/Crp Evaluation
  trial JAMA 200128664-70. And other trials have
  proven that Statins lower CRP 15-25 within 6
  weeks of initiation.
• Weight loss, exercise and smoking cessation also
  lower CRP.

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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.
• How to answer this ?
• 2003 15,000 patients with LDLlt130 but CRP above
  2.0mg/l (JUPITER). All will be put on CRESTOR
  for prevention. What will happen?

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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.
• Review 45 yr old woman with an LDLlt130 but FHX
  and other borderline riskseg a 5 Framingham
  risk
• HOW about checking an hs-CRP to further assess
  her risk ?

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Case 4 Middle of the Road

• CRP 3.2mg/l HIGH risk
• Studies have proven she is in fact at risk more
  than her LDL would tell us. What to do?
• Smoking cessation will lower CRP
• Statins will lower her CRP
• But, no prospective proof that this will change
  her outcome. It is your call, Doctor!

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Other Novel Risk Factors

• EBCT (coronary Ca score)
• Lp (a) lipoprotein, Apo B, LDL particle size
• Homocysteine
• Plasma Adiponectin

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EBCT/Coronary Ca scores

• Coronary Ca occurs due to ASCVD
• Normal score0-10 11-100 mild disease, 101-400
  non-obstructive disease, gt400 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 it is an alternative.

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EBCT

• Like with hs-CRP, it is not very useful in low
  risk or very high risk patients. It significantly
  correlates w/ cheaper hs-CRP.
• Best used in intermediate risk folks where it
  might change treatment approach.
• In patients w/ intermediate risk an EBCT score
  gt80 has a sensitivity of 85 and a specificity of
  75 for the risk of events.

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EBCT/Coronary Ca Scores

• USPSTF Feb 2004 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

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Homocysteine

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

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Homocysteine

• NEJM 13 April 2006 2 studies re homocysteine
  lowering
• 1 Secondary prevention 5522 patients placebo
  vs 2,5mg FolateB6B12 did not reduce the risk
  of cardiovascular event, more pts in Tx had
  unstable angina.
• 2 3749 pts post-MI treatment with B-vitamins
  did not lower risk of recurrent CV disease. A
  harmful effect of B-vitamin Tx was suggested.

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Lipid Sub-fractions other markers

• Lipoprotein a, Apolipoprotein B, LDL particle
  size
• All have predictive value for CHD, indeed LDL
  particle size is more precise than LDL alone. But
  not widely available, expensive, less
  reproducible and still no outcome studies.

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Case 5 The Unreachable Goal

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

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Case 5 The Unreachable Goal

• PE 70 160lbs P60 BP124/76
• Cor RRR, no m/r/g, no jvd, healed median
  sternotomy scar
• Ext no edema
  Lungs slight dec. breath sounds
• TC180, HDL42 TG100 LDL118

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Case 5 The Unreachable Goal

• Risk Assessment he has CHD 2 prev.
• Goal LDL is lt100 per ATP III (lt70-80 TNT trial
  data and ATP update)
• At this level atherogenesis seems to arrest
• At an LDL of 80 in mammalian species
  atherogenesis reverses. Also the PROVE-IT trial
  shows that an LDL of 62 was superior to an LDL of
  95.

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Case 5 The Unreachable Goal

• You decide to increase the simvastatin to 40mg po
  qd.
• 6 weeks later TC 170 TG105 HDL42 LDL107
• What do you do?

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Case 5 The Unreachable Goal

• Many options 1)increase simvastatin to 80 mg or
  change to atorvastatin or rosuvastatin.
• PROBLEM inc risk of side effects and less LDL
  lowering effect as you inc statin doses. For
  every doubling of dose, LDL decreases by only 6
  . A threefold higher dose by 12 and a fourfold
  increase lowers LDL cholesterol by only 18.

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Case 5 The Unreachable Goal

• 2.) Add Ezetimibe 10 mg po qd less chance of
  side effects should help to reach goal LDL
  easily.
• 3.) Intensify diet Ornish Plan add soluble
  fiber, add soy, add omega-3 fatty acids.
• 4.) Be satisfied and await more trials

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Summary

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

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Summary 8 Points

• 3) Better medication options are a help
  Ezetimibe, Advicor, new statins and a cleaner
  understanding of statin side effects
• 4)Attack the metabolic syndrome!! A multi-modal
  treatment plan is best.
• 5) Dont ignore a chance for prevention because
  your patient is gt70 or lt35.

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Summary 8 Points

• 6) hs-CRP is a powerful new tool to predict risk
  especially in those at intermediate risk.
• But, we need prospective proof that lowering
  it will help reduce ASCVD endpoints.
• 7) Try to get to goal anticipate new ATP-IV
  guidelines.

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Thanks for your Attention!