Pharmacotherapy of Hyperlipidemics Flashcards

1
Q

AHA-ACC Cholesterol Guidelines

A
  • Based on whether management is for primary or secondary prevention
  • Primary prevention gets ASCVD risk assessment to determine NEED for statin treatment
  • Secondary prevention gets assessed to determine if they are very high risk and what the GOAL of statin therapy/additional therapy (if needed) is
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ASCVD Risk Assessment - >20 yo w/o ASCVD

A
  • Assess traditional ASCVS risk factors every 4-6 years

* *Consider assessing 30-year or lifetime ASCVD risk based on ASCVD risk factors for adults 20-39 y.o.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ASCVD Risk Assessment - 40-75 y.o. w/o ASCVD

A
  • Assess traditional ASCVS risk factors every 4-6 years

- Assess 10-year ASCVD risk every 4-6 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ASCVS Risk Assessment

A
  • Obtain lipoprotein profile (total chol., LDL, HDL, triglycerides)
  • Race/ethnicity
  • Weight, height
  • Physical activity level
  • Diet (food/alcohol)

Traditional Risk Factors

  • Smoking status (within the last 7 days)
  • Hypertension (>130/80)
  • Low HDL-C (<40 mg/dl)
  • Age and gender (>45 y.o. for men, >55 y.o. for women)
  • Diabetes (hemoglobin A1c)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Risk-Enhancing Factors

A
  • Family history, 1st degree relative, of premature ASCVD (<55 y.o. for men, <65 for women)
  • Primary hypercholesterolemia (LDL 160-189, non-HDL-C 190-219)
  • Chronic kidney disease (eGFR 15-59)
  • Chronic inflammatory conditions (psoriasis, HIV, rheumatoid arthritis)
  • History of premature menopause and pregnancy-associated conditions that increase ASCVD (gestational DM and preeclampsia)
  • High-risk race/ethnicity (South Asian)
  • Metabolic Syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Metabolic Syndrome Risk Factors

A

Requires 3 of the following 5:

  • Fasting glucose>100mg/dL
  • HDL-C <40 mg/dL in males or <50 mg/dL in females
  • TGs >= 150 mg/dL
  • Waist circumference >40 inches in males or >34 inches in females
  • SBP >= 130 mmHg or DBP >= 85 mmHg
  • Receiving anti-hypertensive medicatiosn
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lipid Biomarkers

A
  • Persistently elevated TGs (>= 175 mg/dL)
  • Elevatedhs-CRP >=2 mg/L
  • Elevated Lp(a) >= 50 mg/dL
  • Elevated apoB >= 130 mg/dL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ABI

A
  • Ankle-brachial Index
  • ABI < 0.9 is a risk factor
  • Ratio fo SBP measured at the ankle compared to it measured at brachial artery
  • Typically used as indicator of peripheral arterial disease (PAD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Measuring LDL/Non-HDL Recommendations

A
  • 20 y.o.+ and not on lipid-lowering therapy should have either fasting/non-fasting plasma lipid profile taken to estimate ASCVD risk, also document baseline LDL
  • 20 y.o.+ who are found to have a TG >= 400 mg/dL, a repeat lipid profile in a fasting state should be done to assess fasting TG and LDL levels
  • Assess fasting plasma lipid profile if they have a family history of premature ASCVD or genetic hyperlipidemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Healthy Lifestyle

A
  • Guidelines endorse a healthy lifestyle for everyone
  • Reduces ASCVD risk at all ages, can reduce development of risk factors and is the foundation of ASCVD risk reduction
  • Lifestyle therapy is the primary intervention for metabolic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Lifestyle Management

A
  • Healthier dietary patterns
  • Increasing healthy foods (veggies, fruits, whole grains, low-fat dairy, etc)
  • Limit sweets, sugar-sweetened beverages, red meats
  • Utilize plans such as DASH, USDA food pattern or AHA diet
  • Reduce sodium intake (<2400 mg/day)
  • Increased physical activity: 150 mins per week of moderate-intense exercise or 75 mins per week of vigorous-intensity exercise
  • Healthy weight
  • Stop smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Secondary Prevention: ASCVD not high risk, Age =< 75 y.o.

A
  • High intensity statin, goal of lowering LDL by at least 50%
  • If high intensity statin isn’t tolerated, use moderate intensity statin
  • If on maximal statin therapy and LDL is still >= 70 mg/dL, adding Zetia may be reasonable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Secondary Prevention: ASCVD not high risk, Age >75 y.o.

A
  • Initiate moderate or high level intensity statin

- Continue high-intensity statin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Secondary Prevention: high risk for ASCVD

A
  • High intensity or maximal statin
  • If on maximal statin an LDL is still above 70 mg/dL, adding Zetia may be reasonable
  • If a PCSK9-I is considered, add Zetia to max statin first
  • If on maximal LDL lowering therapy and LDL level is still too high ornon-HDL is >100 mg/dL, adding a PCSK9-I may be reasonable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Very-High Risk of Future ASCVD Events

A

Previous Events

  • Recent acute coronary syndrome within the past 12 months
  • History of MI
  • History of ischemic stroke
  • Symptomatic peripheral arterial disease

Risky Conditions

  • > 65y.o.
  • Heterozygous familial hypercholesterolemia
  • History of coronary artery bypass surgery or percutaneous coronary intervention
  • Diabetes mellitus
  • Hypertension
  • Chronic kidney disease
  • Currently smoking
  • Persistently high LDL levels despite max statin therapy and Zetia
  • History of congestive heart failure

**Need either 2 events or 1 event and 2+ conditions to be considered very high risk)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

High Intensity Statin Therapy

A
  • Goal: daily dose to lower LDL by >50%
  • Atorvastatin 80 mg
  • Rosuvastatin 20 (40) mg

() - titration option

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Moderate-Intensity Statin Therapy

A
  • Goal: lower LDL by 30-50%
  • Atorvastatin 10 (20) mg
  • Rosuvastatin (5) 10 mg
  • Simvastatin 20-40 mg
  • Pravastatin 40 (80) mg
  • Lovastatin 40 mg
  • **Fluvastatin XL 80 mg
  • Fluvastatin 40 mg bid
  • **Pitavastatin 2-4 mg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Low-Intensity Statin Therapy

A
  • **Simvastatin 10 mg
  • Pravastatin 10-20mg
  • Lovastatin 20 mg
  • **Fluvastatin 20-40 mg
  • **Pitavastatin 1 mg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ASCVS not at Very High Risk

A
  • Encourage healthy lifestyle
  • High-intensity statin therapy or maximally tolerated therapy (goal to lower >50%)
  • If high-intensity can’t be tolerated attempt moderate-intensity
  • If on maximally tolerated statin therapy and LDL is still too high, add Zetia
  • If patient is >75 y.o., initiate moderate or high intensity (continue high intensity if already on and tolerating)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ASCVS at Very High Risk

A
  • Encourage healthy lifestyle
  • High-intensity statin therapy or maximally tolerated (goal to lower >50%)
  • Add Zetia if necessary
  • Zetia should be added BEFORE PCSK9-I
  • If on maximal LDL lowering (Statin and Zetia) and LDL or non-HDL are still to high, adding a PCSK9-I is reasonable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Primary Prevention: Patients with LDL > 190 mg/dL

A
  • Patients 20-75 years of age with severe primary hypercholesterolemia - high intensity statin therapy or maximally tolerated statin therapy
  • If <50% reduction of LDL or LDL remains higher than 100 mg/dL, add Zetia
  • If <50% reduction of LDL occurs while on a statin + Zetia, BAS may be considered
  • If LDL levels still remains high on statin + Zetia and the patient has multiple factors that increase subsequent risk of ASCVD events, a PCSK9 inhibitor may be considering (long term safety is uncertain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Primary Prevention: Patients with Diabetes

A
  • 40-75 y.o. with DM and high LDLs, start moderate-high statin therapy
  • High risk ASCVD DM patients. especially those with multiple RFs or 50-75 y.o., use high-intensity statin therapies
  • IF 10-year ASCVD risk >=20% and has <50% decrease in LDL on maximal statin, add Zetia
  • If older than 75 y.o., start statin therapy after a discussion or continue therapy if already on it
  • 20-39 y.o. with DM risk enhancers, initiate moderate intensity statin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Diabetes-Specific Risk Enhancers

A
  • Long duration (over 10 years for type 2, over 20 years for type 1)
  • Albuminuria >= 30mcg of albumin/mg creatinine
  • eGFR < 60 mL/min/1.73 m^2
  • Retinopathy
  • Neuropathy
  • ABI< 0.9
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Primary Prevention: 40-75 y.o., no DM, LDL 70-189 mg/dL (Based on ASCVD Risk Assessment)

A
  • Risk <5% (Low Risk) - Emphasize lifestyle changes to reduce risk factors
  • Risk 5-7.5% (Borderline Risk) - If risk enhancers present, discuss moderate intensity statin, CAC may help with decision process
  • 7.5-20% (Intermediate Risk) - if risk estimate and enhancers favor statins then prescribe moderate intensity statin (if uncertain, consider measuring CAC)
  • > 20% (High Risk) - initiate statin to reduce LDL >= 50%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

CAC Scores

A
  • Coronary Artery Calcium Score
  • If zero, withhold statin therapy and reassess in 5-10 years as long as higher risk conditions are absent
  • If 1-99, start statin therapy for >=55 y.o.
  • If >100 or >= 75th percentile, initiate statin therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

CAC

A
  • Computed tomography of chest
  • Measures amount of calcified plaque in coronary arteries
  • Zero - low risk
  • 1-99 - mild plaque development
  • > 100 - moderate amount of plaque
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Monitoring

A
  • Assess adherence and percentage response to LDL lowering medications and lifestyle changes with repeat lipid measurement 4-12 weeks after statin initiation or dose adjustment
  • Repeat every 3-12 months as needed
  • Define responses to lifestyle and statin therapy by percentage reductions in LDL levels compared with baseline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Primary Prevention: 20-39 y.o.

A
  • 10-year ASCVD risk not available using PCE
  • Can use to estimate Lifetime risk
  • Consider statin therapy if family history of premature ASCVD and LDL >= 160 mg/dL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Primary Prevention: >= 75 y.o.

A
  • If LDL levels between 70-189 mg/dL, initiating a moderate-intensity statin may be reasonable
  • May be able to stop statin therapy when functional decline, multimorbidity, frality, or reduced life-expectancy limits the potential benefits of statin therapy
  • In 76-70 y.o. with LDL 70-189 mg/dL, may be reasonable to measure CAC to reclassify those with a CAC score of zero to avoid statin therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Primary Prevention: Pediatrics

A
  • Children/adolescents with lipid disorders related to obesity, recommend to intensify lifestyle therapy
  • In children >10 y.o. with persistent LDL >190 or >160 with possible FH, not responding to 3-6 mo. of lifestyle therapy, reasonable to start statin therapy
  • IF family history of premature CVD or primary dyslipidemia, reasonable to measure fasting lipid profile as early as 2 y.o. to detect FH or primary dyslipidemias
  • In children w/o CV risk factors of family history of ASCVD, may be reasonable to measure lipid rpofile between 9-11 y.o. and again at 17-21 y.o.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Recommendations for Hypertriglyceridemia, > 20 y.o.

A

-Those with moderate hypertriglyceridemia should have lifestyle factors addressed, secondary factors assessed, and consider medications that increase TGs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Recommendations for Mod-Sev Hypertriglyceridemia, 40-75 y.o.

A
  • ASCVD risk >= 7.5%, reevaluate ASCVD risk after lifestyle and secondary factors are addressed
  • Consider persistently high TG levels as a factor favoring the initiation or intensification of statin therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Recommendations for Severe Hypertriglyceridemia, 40-75 y.o.

A

-ASCVD >= 7.5%, reasonable to address reversible causes of high TGs and initiate statin therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Recommendations for Severe Hypertriglyceridemia (esp fasting TGs >= 1000 mg/dL)

A
  • Reasonable to identify and address other causes for raised TGs
  • Persistently elevated/increasing TGs, reduce TGs with low-fat diet, avoid refined carbs and alcohol, consume omega-3 fatty acids
  • If needed to prevent acute pancreatitis, utilize fibrate therapy
35
Q

Statins

A
  • MOA: inhibit HMG-CoA Reductase, increases hepatic LDL receptors
  • Decreases LDL, decreases TGs, increases HDL
36
Q

Statins reduce…

A
  • Major coronary events and stroke
  • CV-related and total mortality
  • Coronary procedures (PCI/CABG)
  • In general, for every 1% reduction in LDL and 1% reduction of ASCVD event is achieved
37
Q

Cholesterol Treatment Trialists’ Collaborators

A
  • Meta-analysis of 27 statin studies
  • 175,000 patients with and without vascular disease
  • Relative risk per 1 mmol/L LDL reduction based on baseline 5-year CV risk
38
Q

Statin Drug Interactions

A
  • Simvastatin and Lovastatin - CYP3A4 inhibitors (grapefruit juice)
  • Atorvastatin - less first pass metabolism so small increases in concentration
  • Fluvastatin - CYP2C9 metabolism, few interactions
  • Pravastatin and rosuvastatin - not metabolized by CYP
  • Most statins are affected by OATP1B1 inhibitors like gemfibrozil and cyclosporine
39
Q

Safety Summary for Statins

A
  • Excellent patient acceptance
  • Relatively low cost
  • Few SEs: GI most common, high intensity can elevate liver enzymes
  • Myopathy and rhabdomyolysis are also rare possibilities
  • Increases risk of DM
  • Allergies are rare
  • No increases in total or non-CHD mortality
40
Q

Myopathy

A

General term referring to any disease of muscles; can be acquired or inherited and can occur at birth or later in life

41
Q

Myalgia

A

Muscle ache or weakness without creatine kinase elevation

42
Q

Myositis

A

Muscle symptoms with increased CK levels

43
Q

Rhabdomyolysis

A

Muscle symptoms with marked CK elevation (>10x the upper limit), usually accompanied with brown urine.

44
Q

Safety Reccs BEFORE starting Statins

A
  • Counsel patient on healthy lifestyle
  • Obtain baseline ALT
  • Obtain baseline CK and indicateifthere is a family history/past history of myopathy
  • Determine baseline muscle pain or weakness
  • Obtain HgbA1c, if not already collected
  • Determine baseline confusion/memory state
45
Q

Safety Reccs while taking Statins - Myopathy

A
  • Monitor for myopathy with each visit
  • If myopathy is severe (intolerable), D/C statin and check CK, creatinine, and a urinalysis
  • Mild-moderate symptoms: D/C statin and check CK, if CK <10x ULM lower the strength of the same statin then D/C if symptoms recur
  • IF after 2 months of no statins, symptoms or elevated CK do not improve, consider other muscle problem and restart statin
46
Q

Safety Reccs while taking Statins - Liver Toxicity + Others

A
  • Monitor for liver toxicity (weakness, loss of appetite, abdominal pain): if present, measure hepatic function
  • Evaluate for new-onset DM
  • IF experiencing confusion/memory worsening, evaluate for nonstatin causes
  • CI: pregnancy, lactation
47
Q

Statin Counseling

A
  • Take at the same time everyday (Lova, sim, and fluva to take a bedtime)
  • Report unexplained muscle pain, tenderness, or weakness
  • Report symptoms of liver dysfunction
  • Check lipid profile 4-12 weeks following starting statin, then periodically
  • May cause stomach upset or headache, usually goes away from 1-2 weeks
  • Drug interactions
48
Q

BABs

A
  • MOA: block reabsorption of bile acids in the intestine which causes the liver to convert more cholesterol into bile (increases LDL receptors)
  • 15-30% reduction in LDL; increase HDL 3-10%, INCREASES TGs 0-12%
  • Reduce major coronary events and CHD deaths
  • Adverse effects: GI (bloating and constipation), increases TGs
  • Absolute CI: biliary obstruction, fasting TGs > 300 mg/dL (possibly if ranging from 250-299 as well)
49
Q

BAB Drug Interactions

A

-Decreases absorption of anionic drugs (cyclosporine, phenytoin, glimeperide, warfarin, fat-soluble vitamins, etc.)

50
Q

BAB Dosing/Monitoring

A
  • Cholestyramine: 4-24 gm/d
  • Colestipol: 5-30 gm/d
  • Colesevelam: 3.8-4.2 gm/d

Monitoring: Fasting lipid profile 3 months after starting and then every 6-12 months. CBC yearly.

51
Q

BAB Counseling

A
  • Start low and titrate dose up gradually
  • Split doses (BID)
  • Drink plenty of fluids
  • If a powder, mix with at least 6oz of juice or water, mix slowly to avoid foaming, and refrigerate to help the taste
  • Take before or with meals
  • Mix with psyllium to help with constipation
52
Q

Zetia

A
  • Selective cholesterol absorption inhibitor
  • Binds to NPC1L1
  • Dose: 10 mg QD
  • Available in combination with simvastatin
  • Decreases LDL 15-20%, increases HDL 4-9% as monotherapy and a add-on
  • No data on CV morbidity or mortality
  • No effect on blood levels of fat soluble vitamins
53
Q

Zetia Monitoring

A
  • Lipid profile 4-12 weeks after starting
  • May increase risk of liver enzyme elevation when used with statins, so obtain baseline of these levels and repeat if symptoms arise
54
Q

IMPROVE-IT

A
  • Vytorin (Zetia+Zocor) v.s. Zocor in 18,144 patients with ACD for a median of 7 years
  • Lowered LDL more as a combo than zocor alone
  • Reduced CV-related death by 6.4%
  • 2.0% risk reduction overall compared to the Zocor alone
55
Q

Evolocumab (Repatha)

A
  • PCSK9-I
  • Approved in 2015 to be used with a diet
  • Reduces risk of CV events
  • Recommended for those on maximally tolerated statin therapy or other LDL lowering therapies who need additional LDL lowering
  • Dosing: 140 mg SC q2w, OR 420mg SC monthly
  • EXPENSIVE
56
Q

Fourier Study

A
  • 27,564 patients with ASCVD and on high-intensity statins
  • Added Evolocumab at one of the specified dosing and placebos
  • LDL decreased by 59%
  • CV-related deaths decreased by 15%
57
Q

Alirocumab (Praluent)

A
  • PCSK9-I
  • Approved in 2015 to be used with a diet and maximally tolerated statin therapy with inherited hypercholesterolemias
  • Dose: 75 mg SC q2w, can increase dose to 150 mg if response if insufficient
  • EXPENSIVE
  • Store in fridge, let warm to room temp for 30-40 minutes before injection
58
Q

Odyssey Outcomes Trial

A
  • 18,924 patients with recent ACS on max tolerated atorvastatin or rosuvastatin with high LDL or non-HDL
  • CV-related deaths decreased by 15%
59
Q

PCSK9-I Comparison

A
  • Similar efficacy in terms of LDL reduction (45-70%)
  • Monotherapy or add-on
  • SE have been minimal
  • Nasopharyngitis, injection site reactions, and influenza
60
Q

Omega-3 Fatty Acids (Fish Oil)

A
  • Effective at lowering TGs (25-30%), increase LDL (5-10%), especially at high doses
  • Minimal effects on HDL
  • MOA: not understood, possibly increases plasma LPL and decreases hepatic lipogenesis
  • Showed to decrease CHD events
61
Q

Omega-3 Fatty Acids (Drug Examples)

A
  • Lovaza - 960gm per capsule: indicated for TGs > 500 mg/dL, 4 grams daily
  • Vescepa - 1gm per capsule: indicated TGs > 500 mg/dL, dose 2 gm BID
  • Epanova - approved for TGs > 500 mg/dL, dose 2 gm or 4 gm daily
  • Max EPA: 1 gm/capsule, titrate to max of 4gm/day (12 capsules)
62
Q

Omega-3 SE

A
  • At higher doses can effect bleeding time
  • May impair insulin secretion
  • GI: nausea, diarrhea, eructation, taste disturbance
63
Q

REDUCE-IT Trial

A
  • 8,179 patients with ASCVD or diabetes and additional CV RFs on statins with elevated TGs and LDL
  • Primary EP: composite of CV death, nonfatal MI, nonfatal stroke, coronary revascularization, or unstable angina
  • Median follow-up: 4.9 years
  • Results: Primary EP occured 17.2% of Vescepa patients (5% less than placebo), CV death also decreased
64
Q

Fibric Acid Derivatives

A
  • Activation of PPAR(alpha), lipolysis and increases LPL activity which decreases serum VLDL and upregulates ApoA1 which increases HDL
  • Decreases TGs 30-50%, increases HDL by 10-20%, may slightly increase OR decrease LDL
  • Reduces major coronary CV events by 10% with no effect on CV mortality
  • Adverse effects: GI upset, gall stones, hepatotoxicity, myopathy, neutropenia, thromboembolism
65
Q

Fibric Acid Monitoring

A
  • LFTs at baseline, 6-12 weeks, then about q3 months
  • Serum creatinine and eGFR at baseline, 3 months, and q6m
  • CBC at baseline then periodically
  • Baseline CK
66
Q

Fibric Acid CI

A
  • Hepatic dysfunction
  • Severe renal disease
  • Gallbladder disease
67
Q

Fibric Acid Drug Interactions

A
  • Warfarin (increase PT/INR)
  • Statins (increase myopathy)
  • Cyclosporine (increases [fibrate])
  • *Don’t use gemfibrozil with statins, fenofibrate okay with low-moderate intensity statins**
68
Q

Fibrate Patient Counseling

A
  • Report unexplained muscle pain, tenderness, weakness
  • Report severe abdominal pain
  • Lipid profile (4-6 weeks after starting, then periodically), liver enzymes (LFT baseline, 6-12 weeks after, then q3mo), and kidney function (SCr and eGFR baseline, 3 mo later, then q6mo)
  • May cause stomach upset which should stop after 1-2 weeks
  • Drug interactions
69
Q

Niacin

A
  • MOA: reduces hepatic VLDL synthesis which reduces LDL and TGs
  • Decreases LDL 5-25%, TGs 20-50%, increases HDL 15-30% with crystalline (less with SR)
  • Reduces major coronary events and possibly mortality
  • Adverse Effects: flushing, pruritis, skin rash, abdominal pain, hepatotoxicity, hyperglycemia, hyperuricemia
70
Q

Niacin Monitoring

A
  • FBG or Hba1c, uric acid (baseline and q6mo)
  • Hepatic enzymes (baseline, monthly during dose stabilization, q3mo for first year on SR or at dose threshold for IR/ER)
  • Check LFTs q6mo
71
Q

Niacin CI/DI

A

CI

  • Relative: DM, gout, peptic ulcer
  • Absolute: liver disease (don’t use if enzymes at 2-3x ULN), new onset atrial fibrillation

-DI: Statins (increased risk of myopathy)

72
Q

Niacin Dosing

A
  • Start low and go slow
  • IR: 100 mg TID x 1w, 250 TID x1w, 500mg TID x1w then assess. Can increase to 750 mg TID and then 100mg TID if needed
  • ER: 500mg qhs x4w, then 1000mg QHS, may increase to 2000 mg if needed
  • SR: 250 mg BID then increased weekly to 1.5-2gm
73
Q

Niacin Counseling

A
  • Slow titration
  • Take with low-fat snack or meal
  • Administer aspirin (325mg) 30 minutes prior to first dose of niacin if no CIs
  • Take at bedtime (SR or ER)
  • Avoid other vasodilatory activities (alcohol, hot beverages, spicy foods, hot showers/baths, vigorous physical activity)
74
Q

Red Yeast Rice

A
  • Activity against HMG-CoA Reductase
  • Lowers LDL 20-25%
  • Counsel on the need for monitoring
  • Linked to myopathy, hepatotoxicity, and rhabdomyolysis
75
Q

Chinese Coronary Secondary Prevention Study

A
  • Showed Red Yeast Rice significantly reduced CV events, CV mortality, and total mortality
  • Studied 4,870 patients for 4.5 years
  • Capsules used contained a combination of lovostatin, ergosterol, and other components
76
Q

Psyllium Husk

A
  • Metamucil

- Good, lowers LDL 10-15%

77
Q

Garlic

A
  • Probably good

- Lowers LDL 2-3 mg/dL

78
Q

Olestra

A
  • “WOW”
  • Not so good
  • TC lowered 5-8%
79
Q

Policosanol

A

-Not good in controlled clinical trials

80
Q

Guggalipid

A

-Controlled trials weren’t impressive

81
Q

Cinnamon

A
  • Goof

- Lowered LDL 9 mg/dL

82
Q

Green Tea Extract

A
  • Good

- Lowered LDL 5 mg/dL

83
Q

Almonds

A
  • Good

- Lowered LDL 6 mg/dL

84
Q

Plant Stanols/Sterols

A
  • Good

- Lowered LDL 12 mg/dL