Transcript Document

Hyperlipidemia
Saudi Diploma in Family Medicine
Center of Post Graduate Studies in Family Medicine
Presented by: Dr. Zekeriya Aktürk
[email protected]
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% .
•The overall prevalence of hypertriglyceridemia
TG > 150 mg/ dL) : 49.6%.
•HDL Values in men and women
Men <40mg/dL: 74.8 %
Women <50mg/dL: 81.8
Al-Nozha MM.et al. Metabolic syndrome in Saudi Arabia. Saudi Med J 2005; 26 (12): 1918-1925
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 body’s
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; deepfried 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 > 200 or HDL <40, 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
– < 100 →Optimal
– 100-129 → Near
optimal
– 130-159 → Borderline
– 160-189→ High
– ≥ 190 → Very High
• Total Cholesterol
– < 200 → Desirable
– 200-239 → Borderline
– ≥240 → High
• HDL
– < 40 → Low
– ≥ 60 → High
• Serum Triglycerides
–
–
–
–
< 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 antihypertensives)
• 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, 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
LDL (15-30),  HDL (15-35)
 Triglyceride (20-50)
Nicotinic Acid
Fibric Acids
Gemfibrozil
Fenofibrate
Bile Acid sequestrants
Cholestyramine
LDL (5-20), HDL (10-20)
Triglyceride (20-50)
 LDL
 HDL
No change in triglycerides
Flushing, Hyperglycemia,
Hyperuricemia, GI distress,
hepatotoxicity
Dyspepsia, gallstones,
myopathy
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 patient’s 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 patient’s 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 nation’s #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 < 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 < 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)
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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, HDL<40 or >60)
• 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
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Framingham Ten Year Risk
0
3
Non-Smoker
0
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Framingham Ten Year Risk
0
3
0
1
HDL = 43
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Framingham Ten Year Risk
0
3
0
1
0
SBP = 119, untreated
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
CHD/10yr <100mg/dl
risk>20%
(high)
2+RF or
<130mg/dl
10yr<20%
(Medium)
0-1 risk
<160mg/dl
factors (low)
Start
T.L.C.
Start Drug
Treatment
>100mg/dl
>100 –
129mg/dl
>130mg/dl
>130 –
160mg/dl
>160mg/dl
>160 –
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190mg/dl
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” 43:2001,pp43-48 and 2003;1;77-79.
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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 >7.5 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, >$$
• If combining w/ a statin use fenofibrate;
gemfibrozil has > 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-3’s; 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 (transaminases>3x nl.) = 0.5%
- rhabdomyolysis = rare; incidence rates per
million Rx’s: 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/ CrCl<30cc/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 (meanLDL=62) had 16%
less of all CV events. 28% less mortality
than pravastatin group (meanLDL=95)
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PROVE-IT Trial
• WOW!
• Evidence from mammalian species had
shown that atherogenesis stops & reverses
at an LDL <80 – now some clinical
outcome data.
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NCEP Update 13 July 2004
• Circulation 13 July 2004:227-239
• Added the results of PROVE-IT, HPS, PROSPER,
ALLHAT, 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; LDL <100 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
HIGH
>20% 10yr
Mod. High
10-20%
Moderate
<10% 10yr
LOW
<70mg/dl >100mg/dl >100mg/dl
or <100mg
Optional
<100mg/dl >130mg/dl >130mg/dl
or 100-130
Optional
<130mg/dl >130mg/dl >160mg/dl
<160mg/dl
TLC
>160mg/dl
DRUGS
>190mg/dl
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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)
• 10,001 patients; 2 groups for 4.9 years with
mean LDL = 99mg/dl before study
– 10 mg atorvastatin (mean LDL=101mg/dl)
– 80 mg atorvastain (mean LDL=77mg/dl)
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TNT - Results
• Side Effects: increased LFT’s 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
<80 versus group with LDL=101.
• More evidence to lower our LDL goals…
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NCEP/ATP III – Step 8
• Identify Metabolic Syndrome: (3 of 5)
– SBP>130, FBS>110, TG>150, HDL<40 in men
and <50 in women, waist>40”men, 35”women
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 (>150mg/dl)
– First lower LDL; if TG still >200 consider
adding/increasing drug therapy
– But, if TG >500mg/dl, first lower triglycerides
to prevent pancreatitis. When they are <500
then return to LDL lowering
– Treat HDL <40 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 HDL=48 TG = 155 LDL = 124
• PMHx: negative, smoker
• Meds: daily vitamin
• FHx: MI in F age 60, M age 64
• PE: 65” 130lbs P=72 BP=118/68
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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. <130
• But, concerns remain: FHx, Smoking, HDL
is <50 & TG >150; both less than ideal.
• What do you do with this “middle-of-theroad” 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.
• < 1mg/l = low risk
• 1-3mg/l = moderate risk
• >3mg/l = high risk
• >10mg/l = invalid for cardiac risk
prediction;consider 1° inflammatory
disease, trauma, serious infection.
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Case #4 – Middle of the Road
• PRINCE (PRavastatin INflammation/Crp
Evaluation trial; JAMA 2001:286;64-70.
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 LDL<130 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
LDL<130 but +FHX and other borderline
risks…eg 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 score=0-10; 11-100 = mild disease, 101400 = non-obstructive disease, >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; 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 >80 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 Folate+B6+B12: did not
reduce the risk of cardiovascular event,
more pts in Tx had unstable angina.
• #2: 3749 pts post-MI: “treatment with Bvitamins 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 P=60 BP=124/76
• Cor: RRR, no m/r/g, no jvd, healed median
sternotomy scar
• Ext: no edema
Lungs: slight dec. breath sounds
• TC=180, HDL=42 TG=100 LDL=118
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Case # 5 – The Unreachable Goal
• Risk Assessment = he has CHD; 2° prev.
• 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. 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 TG=105 HDL=42
LDL=107
• 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) Don’t ignore a chance for prevention
because your patient is >70 or <35.
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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!
85 / 29