Download Hyperlipidemia Management of Patients in the Primary Care Setting

HYPERLIPIDEMIA:
MANAGEMENT OF PATIENTS IN THE
PRIMARY CARE SETTING
Lauren A. Winkler, DNP, RN, FNP-BC
STATISTICS
 Dyslipidemia is one of the key risk factors for development
of CHD
 31.7% of Americans have elevated serum cholesterol levels
 1 in 3 Americans have elevated LDL levels
 31 million Americans have total cholesterol valuesof 240mg/dl or
greater and are considered at high risk of CHD
 39.8% of adult Indiana state residents have elevated
cholesterol levels
CHOLESTEROL PATHOPHYSIOLOGY
 A type of lipid
 Essential components to human cell membranes
 Precursor in steroid hormone and bile acid metabolism
 Transportation of Cholesterol in the form of lipoproteins
 5 Types of Lipoproteins

LDL (Low Density Lipoprotein)

HDL (High Density Lipoprotein)

VLDL (Very-low-density Lipoprotein)

IDL (Intermediate-density Lipoproteins)

Dietary Apolipoproteins
TYPES OF LIPOPROTEINS
 LDL (Low Density Lipoprotein)- Prominent role in CVD risk!

60-70% of circulating total cholesterol
 HDL (High Density Lipoprotein)

20-30% of total cholesterol
 VLDL (Very-low-density Lipoprotein)

10-15% of total cholesterol
 IDL (Intermediate-density Lipoproteins)
 Apolipoproteins

6 major classes

Apo B- increased levels linked to heart disease risk
TRIGLYCERIDES
 Type of Lipid
 Store unused calories
 Provide energy to body
 Circulate body via transportation by lipoproteins
 Biomarker for cardiovascular risk
DYSLIPIDEMIA
 A result of abnormal
lipoprotein metabolism
 Elevated cholesterol level
increases risk for:
 Atherosclerosis
 Coronary Heart Disease
 Presence of atherosclerosis
qualifies as high risk for:
 CHD
 Symptomatic CAD
 PAD
 AAA
PRIMARY ETIOLOGY OF DYSLIPIDEMIA
 Genetics
 Single gene mutations result in faulty apolipoproteins,
receptor, or enzyme resulting in disturbance of
production and clearance in LDL, HDL, and triglycerides.
 Suspect in patients with premature CHD or with family
hx of ASD and total cholesterol >240
FAMILIAL HYPERCHOLESTEROLEMIA
Two types:
 Heterozygous
 Common (1:250)
 Homozygous
 Rare (1:160,000- 1 million)
 LDL >600
 Untreated die in 20’s
 Treated, CAD in 30’s
SECONDARY ETIOLOGY OF DYSLIPIDEMIA
 Diet and exercise play a role in the cause and treatment of
lipid disorders; Sedentary lifestyle.
 Diet: saturated fats and trans-fatty acids, caloric excess,
alcohol.
 Obesity: associated with elevated triglycerides, physical
inactivity with low HDL.
 Endocrine disorders
 Renal disorders
 Hepatic disorders
 Immunologic disorders
 Medications
DRUGS ASSOCIATED WITH DYSLIPIDEMIA
 Diuretics
 Beta blockers
 Anabolic steroids
 Corticosteroids
 Estrogens and androgens
 Retinoids
 Cyclosporine
 Protease inhibitors
 Atypical antipsychotics
MAJOR RISK FACTORS FOR DYSLIPIDEMIA
 Overweight/ Obesity –> most predictive of dyslipidemia
 Family hx (parent w/ TC >240)
 Family hx of premature CHD
 Diabetes Mellitus
 Metabolic Syndrome*
 Cigarette Smoking
 Hypertension
 Low HDL (<40)
 Age: males > 45, females >= 55
CHOLESTEROL SCREENINGS
Pediatrics
 Age 2-8yr only if risk
factors for premature
CVD
Adults
 Every 4-6 years in patients
aged 20-79 without ASCVD
 ACC/AHA 2013
 Once between age 9-
11yr
 Once between age 17-
21yr
 Previously- dependent upon
age, sex, risk factors
ATP III LDL, TOTAL, AND HDL
CLASSIFICATION
 LDL Cholesterol (mg/dl)
 <100
Optimal
 100-129
Near/Above Optimal
 130-159
Borderline High
High
Very High
 160-189
 >190
 Total Cholesterol (mg/dl)
 <200
 200–239
 >240
Desirable
Borderline high
High
 HDL Cholesterol (mg/dl)
 <40
Low
 >60 High (good)
ATP III LDL, TOTAL, AND HDL
CLASSIFICATION
 LDL Cholesterol (mg/dl)
 <100
Optimal
 100-129
Near/Above Optimal
 130-159
Borderline High
High
Very High
 160-189
 >190
 Total Cholesterol (mg/dl)
 <200
 200–239
 >240
Desirable
Borderline high
High
 HDL Cholesterol (mg/dl)
 <40
Low
 >60 High (good)
UPDATED TREATMENT GUIDELINES
 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to
Reduce Atherosclerotic Cardiovascular Risk in Adults
 Lack of evidence to support treating to LDL-C or non-HDL-c targets
 Calculate 10-year ASCVD risk using the Pooled Cohort Equations
Cardiovascular Risk Calculator
 Focus on ASCVD risk reduction: 4 Statin benefit groups
STATIN BENEFIT GROUPS
① Patients with clinical ASCVD
② Patients with primary elevations of LDL-C >190 mg/dl
③ Patients with diabetes aged 40-75 years with LDL-C 70-189mg/dl and
without clinical ASCVD
④ Patients without clinical ASCVD or diabetes with LDL-C 70-189 mg/dl
and estimated 10-year ASCVD risk .7.5%
CV RISK ASSESSMENT CALCULATION
 ACC/AHA 2013 ASCVD Risk Calculator
1. PATIENTS WITH CLINICAL ASCVD
 Includes:
 Acute coronary syndromes
 History of MI
 Stable or unstable angina
 Coronary or other arterial
revascularization
 Stroke or TIA
 Peripheral arterial disease
presumed to be of
atherosclerotic origin
 Age < 75yr and no safety
concerns: High-intensity statin
 Age >75 yr or safety concerns:
Moderate-intensity statin
2. PATIENTS WITH PRIMARY ELEVATIONS
OF LDL-C >190 MG/DL
 Rule out secondary causes of
hyperlipidemia
 Age > 21yr: High intensity statin
 Goal of 50% reduction in LDL-C
 LDL-C lowering non-statin may
be considered to further reduce
LDL-C
3. PATIENTS AGED 40-75 YR WITH
DIABETES AND LDL-C 70-189MG/DL AND
WITHOUT ASCVD
 Moderate intensity statin
 Consider high-intensity statin
when > 7.5% 10yr ASCVD risk
 Adults <40yr or >75 or with
LDL<70mg/dl: evaluate
risks/benefits/patient
preferences when deciding to
initiate, continue, or intensify
statin therapy
4. PATIENTS WITHOUT ASCVD OR
DIABETES WITH LDL-C 70-189MG/DL AND
ESTIMATED 10-YEAR ASCVD RISK > 7.5%
 Calculate risk assessment every 4-6 years in those not receiving statin
therapy
 Re-emphasize heart-healthy lifestyle habits and:
 Adults 40-75yrs with calculated 10-yr ASCVD risk of >7.5%:
Moderate or high-intensity statin
 Calculated 10-yr ASCVD risk of 5 - < 7.5%: Consider moderate-
intensity statin
 Initiation of statin therapy may be considered for adults with LDL-C
> 160mg/dl or other evidence of genetic hyperlipidemias, family
history of premature ASCVD, hs-CRP> 2.0mg/L, CAC score > 300
Agatston units
LOW, MODERATE, AND HIGH INTENSITY
STATINS
Low Intensity
Moderate Intensity
Daily dose lowers LDL-C
on average by <30%
Daily dose lowers LDL-C Daily dose lowers LDL-C
on average by approx. 30- on average by approx.
<50%
>50%
Simvastatin 10mg
Pravastatin 10-20mg*
Lovastatin 20mg*
Fluvastatin 20-40mg
Pitavastatin 1mg
Atorvastatin 10*-20mg
Rosuvastatin 5-10*mg
Simvastatin 20-40mg*
Pravastatin 40*-80mg
Lovastatin 40mg*
Fluvastatin XL 80mg
Fluvastatin 40mg BID*
Pitavastatin 2-4mg
(ACC/AHA, 2013)
High Intensity
Atorvastatin 40-80mg*
Rosuvastatin 20-40mg*
STATINS: LDL LOWERING RATES
Lovastatin
Mevacor
20mg=29%
40mg=31%
80mg=48%
Pravastatin
Pravachor
10mg=19%
20mg=29%
40mg=34%
80mg=48%
Simvastatin
Zocor
10mg=28%
20mg=35%
40mg=40%
80mg=48%
20mg=17%
40mg=23%
80mg=33%
Fluvastatin
Lescol
Atorvastatin
Lipitor
10mg=38%
20mg=46%
40mg=51%
80mg=54%
Rosuvastatin
Crestor
5mg=43%
10mg=50%
20mg=53%
40mg=62%
1mg=30%
2mg=36%
4mg=45%
Pitavastatin
Livalo
• Contraindications: Active or chronic liver disease, pregnancy (Cat.X),
lactation
• Use with caution: Age >75yr, concomitant use of cyclosporine,
erythromycin, itraconazole, ketoconazole, fibric acid, diltiazem, verapamil,
fluoxetine, nefazodone, gemfibrozil, niacin, antifungal agents
STATINS
 Recheck fasting lipids 4-12 weeks after statin initiation, then every 3-12 months
 Doses should be adjusted at 6-week intervals
 Baseline LFTs: If normal, no longer need to monitor LFTs on scheduled bases






clinician judgment
Baseline CK measurement may be warranted if increased risk
Advise patient to stop therapy and order creatinin kinase if patient reports
muscle discomfort, weakness, or brown urine.
Decrease dose when 2 consecutive values of LDL-C are <40mg/dl
Pravastatin and Rosuvastatin metabolism are least affected by other drugs.
Atorvastatin and Fluvastatin do not requiring renal dosing
Do not take at same time as grapefruit juice
Evening vs. morning dosing?
 Adverse effects





Elevated hepatic transaminase
Myopathy
Upper & lower GI complaints
Use with anticoagulant may increase prothrombim time
Older females: new onset diabetes?
MANAGEMENT OF HYPERLIPIDEMIA
 Heart Healthy Lifestyle Habits
 Emphasize reduction in saturated fat & cholesterol
 Encourage moderate physical activity
 Consider referral to a dietitian
 Healthy food changes
 Weight reduction
 Physical activity
 Smoking cessation
 Limit alcohol
EZETIMIBE (ZETIA)
 First-line non-statin medication therapy to consider
 Zetia: 10 mg once daily
 Effects:






18% LDL decrease
1% HDL increase
8% TG decrease
(25% LDL decrease when added to statin)
Contraindication: Hepatic insufficiency
Pregnancy category C
Adverse effects: Upper & lower GI complaints, myopathy, fatigue
Ezetimibe + simvastatin = Vytorin
Ezetimibe + atorvastatin =Liptruzet
**No indication of improved outcomes with ezetimibe
BILE ACID SEQUESTRANTS
 Cholestyramine (Questran Light): One 5-g packet or scoop 1-2 times/day (max
4-6 packs or scoops/day in 2-3 divided dose)
 Colestipol (Colestid): 5-g packet or scoop 1-6 pkts/scoops per day in divided
doses or
Tablets: 2-g 1-2 times/day and increasing by 2-g 1-2 times/day at 1-2
month intervals (max 16-g/day)
 Colesevelam HCL (Welchol): 3 tabs BID (4-6 tabs daily if addition to statin)
Lipid effect
LDL decrease 15-30%
HDL increase 3-5%
TG no change or increase
Contraindications: Familial dysbetalipoproteinemia
Caution: Triglycerides>300
Pregnancy Category C
Side Effects: Constipation, flatulence, nausea, decreased vitamin/medication absorption,
elderly=risk of fecal impaction
NICOTINIC ACID
 Effect:
 Lowers total cholesterol and triglycerides
 Increases HDL (22-26%)
 Niaspan
 >16 years; 500 mg HS for 4 weeks, then
1 g daily for weeks 5-8, then titrate to patient response & tolerance; do not increase
by more than 500mg in a 4 week period; max 2g/day
• Labs – LFT, BG, & uric acid
• Caution - Gout, DM, hyperuricemia, pregnancy category C
• Side Effects-Flushing, hypotension, nausea, gout, elevated blood sugar
levels, hepatotoxicity
FIBRIC ACID DERIVATIVES OR FIBRATES
 To lower serum triglycerides
 Lipid effects
LDL decrease 5-20%
HDL increase 10-20%
TG decrease 20-50%
 Gemfibrozil: 600mg BID 30 mins before AM & PM meals
 Fenofibrate (Tricor, Lipofen, Lofibra): 40-160mg daily; adjust @ 6-8 wk intervals (max





160mg/day)
Fenofibric acid (Fibricor, Trilipix): 35-105mg PO daily; adjust dose q4-8 weeks
Labs- Liver function tests
Contraindications- Severe renal or hepatic disease
Caution-Hx gallstones; increased risk of rhabdomyolysis with statins; potentiates
effects of anticoagulants
Side Effects-Dizziness, dyspepsia, diarrhea, blurred vision
OMEGA-3 FATTY ACIDS
(LOVAZA, VASCEPA)
 Combination of EPA and DHA omega-3 fatty acids, 1 gram capsules
 Adjunct to diet
 Only for severe hypertriglyceridemia (>500mg/dl)
 Reduces triglycerides 45%
 Raises HDL 9.1%
 Raisess LDL 44.5%
 Dosage: 4gm/day
 Caution: fish and shellfish allergies, may increase bleeding times
 Side effects: Belching, “fishy” taste in mouth
PCSK9 INHIBITORS
 Praluent (alirocumab)
 Repatha (evolocumab)
 Mechanism of action: PCSK9-specific antibodies block degradation of
LDL receptors in the liver, causing the liver to clear plasma levels of
LDL-C
 Indications:
 Goals not achieved on maximally tolerated statin and ezetimibe for secondary
prevention or familial hypercholesterolemia
 Not recommended for use in primary prevention patients in the absence of familial
hypercholesterolemia*
 Dosing:
 Repatha (evolocumab): 140mg SC q2wk / 420mg SC qmonth [~$14,100/year]
 Praluent (alirocumab): 75mg SC q2wk [~$14,600/year]