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Year 3 - Clinical > 16 - Dyslipidemia > Flashcards

16 - Dyslipidemia Flashcards

1
Q

Describe the “lipid profile”

A
  • Variability in cholesterol test = 7-11%; cholesterol changes < 7% w/ a statin dose increase
  • “Healthy” values:
    • Total cholesterol < 5.2 mmol/L
    • LDL < 3.4 mmol/L
    • HDL > 1 (men) > 1.3 (women)
    • TG < 1.7 mmol/L
  • No longer recommended to fast for tests
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2
Q

What is the role of LDL, HDL, and triglycerides?

A
  • High levels of LDL promotes buildup of plaque in the artery walls
  • HDL helps carry LDL-cholesterol away from artery walls
  • Triglycerides are a type of fat found in the blood; high levels associated w/ excess weight, excess alcohol consumption & diabetes (don’t know if they play a role in cardiac disease)
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3
Q

Hyperlipidemia is an independent risk factor for:

A
  • Coronary heart disease (angina, MI)
  • Cerebrovascular disease (ischemic stroke)
  • Peripheral artery disease
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4
Q

Modifiable risk factors for CVD

A
  • Diet, exercise
  • Smoking
  • Stress
  • Hypertension, dyslipidemia
  • BMI > 27
  • Sedentary lifestyle
  • Excessive alcohol intake
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5
Q

Non-modifiable risk factors for CVD

A
  • Genetics (family history of premature CHD, < 55 if male, < 65 if female; familial hypercholesterolemia, very high cholesterol regardless of diet, very rare)
  • Gender (male)
  • Age
  • Chronic kidney disease
  • Ethnicity
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6
Q

Why should we do a risk assessment for dyslipidemia?

A
  • Identify px most likely to benefit from pharmacotherapy
  • Reassure low risk individuals w/o any treatable risk factors & a healthy lifestyle that they are doing well
  • Advise individuals w/ treatable risk factors or unhealthy behaviours to address these factors
  • Engage px in tx decisions & increase adherence to therapy
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7
Q

Advantages to ASCVD over Framingham

A
  • Broader population
  • Narrower outcomes (easier to translate)
  • Results based on study that looked at chance of dying from a heart attack, chance of having a stroke, & chance of having a non-fatal heart attack
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8
Q

Causes of dyslipidemia

A
  • Genetics (ex: familial hypercholesterolemia)
  • Conditions (type 2 DM, CKD, hypothyroidism, nephrotic syndrome, cholestatic liver disease)
  • Lifestyle (saturated fats increase lipids; refined carbs & simple sugars increase TG; smoking decreases HDL; aerobic exercise increases HDL; moderate EtOH increases HDL)
  • Drugs => drug-induced hypercholesterolemia (progestins, thiazide diuretics, anabolic steroids, beta blockers, isotretinoin)
    • Thiazide diuretics increase TC & LDL 5-10%, and TG 5-15%
    • Beta blockers increase TG 15-50%, less w/ selective BB; also decrease HDL 5-20% but still decrease CVD events & mortality
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9
Q

3 things that can positively affect lipid profile & decrease risk of CV events

A
  • Physical activity
  • Diet (Mediterranean decreases CVD mortality)
    • Can improve Framingham by 30% (but only if pt can commit to this diet for the next 10 years)
  • Stop smoking
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10
Q

Relative risk reduction w/ a statin

A

25-30% reduction in CV events (MI, stroke, CHD death)

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11
Q

What should be considered when determining which statin to use?

A
  • Efficacy & harm = consider them all the same
  • Drug interactions = simvastatin & lovastatin > atorvastatin > pravastatin & rosuvastatin
  • Cost = similar (all available generic)
  • Dose = w/ some exceptions, generally start at equivalent of 10 mg atorvastatin (40 mg lovastatin & pravastatin; 20 mg simvastatin; 5 mg rosuvastatin)
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12
Q

What is the target for statin therapy?

A
  • Guidelines say primary target < 2 mmol/L or >/ 50% decrease in LDL-C (if started as high risk, Framingham >/ 20%)
  • Trials didn’t target LDL, nor did they increase or decrease meds to meet targets, nor did they compare one LDL target to another
  • Summary = don’t target specific lipid levels & don’t repeat lipid level testing for a pt on a statin (no data that changing dose changes relative 10-year CVD risk)
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13
Q

General side effects of statins

A
  • Muscle pain (myalgia)
  • Upper GI (diarrhea, nausea, dyspepsia), sleep disturbances ~ 5-10%
  • New onset type 2 DM (very rare, don’t mention to pt)
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14
Q

Effect of statins on aminotransferases

A
  • > 3x ULN occurs in < 2-3% of px on statins (NNH = 250)
  • Liver failure RARE (less than 2/million px/year)
  • Get a baseline; no follow-up necessary unless concerning sx (ex: dark urine, upper abdominal pain, N/V, yellowing of skin or eyes, general itchiness, pale stools)
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15
Q

Describe statin associated muscle complaints

A
  • Usually starts in larger muscles
  • Diffuse (not unilateral)
  • Onset about 1-12 months of therapy (or after dose increase/addition of interacting drug)
  • Myalgia = no significant increase in creatinine kinase
  • In practice, 5-10% of statin treated px report muscle complaints
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16
Q

Difference between myositis and rhabdomyolysis

A
  • Myositis = myalgia + CK levels 2-10x ULN; may be caused by strenuous exercise
  • Rhabdomyolysis = severe, progressive muscle aches w/ CK > 3-10x ULN & marked sCr elevation or myoglobinuria
17
Q

What should be done if a pt is on a statin and has new unexplained muscle sx?

A

Ask about other sx and have CK checked

18
Q

The amount of effort spent persevering w/ statin therapy in subjects w/ AEs should be directly related to ____

A

The level of CV risk for the individual pt

19
Q

Management of myalgia

A
  • Hold statin for 1-2 weeks (or until sx resolve) and re-challenge
  • Can use different statin and/or dose reduction OR reassess risk vs. benefit of restarting statin (is the pt high or low risk of CVD, is it primary or secondary prevention)
20
Q

Management of myositis

A
  • If CK > 2-4x ULN but < 10x ULN – D/C statin & follow until sx resolve or CK returns to normal
  • Consider precipitating factors (thyroid, exercise, drug interactions)
  • Reassess risk vs. benefit of restarting statin
  • Change statin and/or reduce dose & titrate up slowly
21
Q

Management of rhabdomyolysis

A
  • Stop statin + hospitalization for supportive tx

- May later rechallenge w/ low dose of different statin (once sx resolved, can take months to years)

22
Q

When should you retest lipids if a pt is not on a statin?

A

2016 CCS dyslipidemia guidelines = CV risk assessment should be completed every 5 years for men & women aged 40-75 y/o or whenever a px expected risk status changes

23
Q

Should statins be used in the elderly?

A
  • Statins should never be started for primary prevention in px > 75 y/o
  • Px > 75 y/o shouldn’t even have their lipids checked
24
Q

Which px are considered “high risk”?

A
  • Framingham score >/ 20%
  • Clinical vascular disease
  • Abdominal aortic aneurysm
  • Diabetes & age >/ 40 y/o or > 15 years duration & age >/ 30 years or microvascular disease
  • Chronic kidney disease
  • High risk hypertension
25
Q

Should statins be used post-MI and in px w/ CAD?

A
  • For px w/ CAD, statins have RRR of CHD event or death of ~25% & ARR of mortality of ~3% (statins considered secondary prevention at this point)
  • High dose (80 mg vs. 10-20 mg atorvastatin equivalent) gave additional 10% RRR (1% ARR) in CHD events or death over 2.5 years
26
Q

What is the effect of adding ezetimibe to statin therapy?

A
  • IMPROVE-IT study looked at over 18,000 post-MI px
  • Intervention was simva 40 mg + ezetimibe VS. simva 40 mg alone x 7 years
  • Results = adding ezetimibe decreased LDL by 15-20%; RRR=6% for CV events, ARR=1.8% for CV death, MI, or stroke
  • No big differences in safety
27
Q

What are PCSK-9 inhibitors and what is their effect on lipids?

A
  • Monoclonal antibodies that inhibit proprotein convertase subtilisenkexin type 9
  • In RCTs, lowered LDL by 50-70%
28
Q

Are PCSK-9 inhibitors used in practice?

A
  • Evolocumab + statin vs. statin alone x 2.2 years decreased LDL by extra 50% (FOURIER trial)
  • Reduced CV events from 5.1% of patients/year to 4.5%
  • However, didn’t reduce deaths
  • Little is known about long-term safety
29
Q

What are some other agents that lower triglycerides?

A
  • Niacin – decrease TG by 20-35% (AIMHIGH study was stopped b/c no decrease in CVD risk)
  • Fibrates – decrease TG by 20-50% (multiple meta-analyses concluded can decrease non-fatal MI by ~10%, but no difference in overall CVD)
  • Omega-3 fatty acids – decrease TG by 25-30% (multiple meta-analyses show no benefit in any CV outcome)
30
Q

What are the effects of TG on pancreatitis?

A
  • High TG are risk factor for pancreatitis
  • JAMA meta-analysis concluded that statins decrease pancreatitis (NNT = 1200 at 5 years); fibrates increase pancreatitis (NNH = 935 a 5 years)

Year 3 - Clinical (30 decks)

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