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IPFC 3 Final > Dyslipidemia Therapeutics > Flashcards

Dyslipidemia Therapeutics Flashcards

1
Q

Define marginal patients. How much % of patients are in this categary.

A

For marginal patients their outcome is dependant on their expose
- 20%

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2
Q

What conditions are high CV risk where treatment is recommended? (4)

A
  • Atherosclerotic CV disease (all 2ndary prevention)
  • CKD
  • DM
  • LDL 5+
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3
Q

What are common conditions of secondary dyslipidemia? (6)

A
  • Excess alcohol
  • Renal failure/Nephrotic syndrome
  • Hypothyroidism
  • Liver disease
  • Pregnancy
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4
Q

What are common drugs of secondary dyslipidemia? (7)

A
  • B-blockers that are NON-selective (propanolol, pindol, labetolol, carvedilol, nadolol)
  • Corticosteroids
  • Antiviral therapy
  • hormone replacement therapy
  • COCs
  • Thiazide diuretics
  • Cyclosporine, carbramazepine, Isotretinoin
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5
Q

In the observational studies, how much did healthy behaviours lower risk of CVD outcomes

A

60-80%

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6
Q

What are the non-pharmacological choices for dyslipidemia

A
  1. Smoking cessation
  2. Healthy diet (mediterranean diet, no trans, saturated fat)
  3. Increase physical activity
  4. 2 or less standard drinks/day or max 9/week for females
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7
Q

What did the nurses’ health study say about having low-risk factors?
Population studied?
Outcome studied?

A

The more healthy lifestyle choices = lower risk of CV outcomes
Population: All women
Outcome: Deaths from coronary heart disease and nonfatal infractions (major coronary events)

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8
Q

What is the % chance of getting an MI if smoking 1 cigarette/day

A

50% higher

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9
Q

Smoking cessation
Studied in primary/secondary prevention?
RRR of CVD risk?
RRR of mortality?
Life expectancy increase by?

A

Studied in secondary prevention, can apply to primary
RRR of CVD risk? 50%
RRR of mortality? 35%
Life expectancy increase by? 10 years

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10
Q

What happens within 1 year of smoking cessation?

A

Risk of Coronary heart disease is about half than a smoker’s

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11
Q

Define surrogate endpoint

A

Certain measurements (physiological, lab results) that are ASSOCIATED with events but are NOT the outcomes themselves

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12
Q

Are CV outcomes dependant on LDL levels?

A

No, only associated
Statins reduced both CV outcomes and LDL

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13
Q

If you target LDL levels without touching the metabolic disorder that caused the high LDL,
decrease/not reduce risk of heart disease? What must you do?

A

not reduce risk of heart
- You must reduce LDL in a WAY that improves the metabolic disorder that caused the high LDL

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14
Q

Which drug is the best for:
Decreasing LDL
Increasing HDL
Decreasing triglycerides

A

Decreasing LDL: Statins, PCSK9s
Increasing HDL: Niacin, fibrates
Decreasing triglycerides: Niacin, Fibrates

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15
Q

Which statins are CYP3A4 inhibitors? (3)

A

Atorvastatin
Simvastatin
Lovastatin

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16
Q

Which statins have the longest half-life? (2)

A

Atorvastatin
Rosuvastatin

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17
Q

Which drug has the lowest risk of interactions?

A

Rosuvastatin

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18
Q

Which drug is metabolized by CYP2C9

A

Fluvastatin
Rosuvastatin (limited)

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19
Q

What are some CYP3A4 inducers and inhibitors?

A

Inducers:
- Carbamazepine
- phenytoin
- omeprazole
- rifampin

Inhibitors:
- Amiodarone
- Diltiazem
- Verapamil
- Azole, grapefruit
- cyclosporine

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20
Q

Which drugs are high-intensity statins?

A

Rosuvastatin 20-40
Atorvastatin 40-80
Simvastatin 80mg

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21
Q

Know a specific dose for primary prevention

A

Know a specific dose for PRIMARY prevention: ROSUVASTATIN 20MG

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22
Q

ASCOT-LLA trial
PICO
RRR

A

Population: Mostly men with HTN + 3 CVD risk factors (total cholesterol over 6.5)

Intervention: Atorvastatin 10mg

O: non-fatal MI and fatal CHD

RRR: 37% reduction in CVD

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23
Q

What are the effects on statins when baseline risk changes such as CV risk score, hypertension, renal dysfunction, diabetes?
What differs?

A

Effects of statins are consistent
- ARR and NNT differs according to baseline risk

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24
Q

What do the trials say for comparing statin treatment dose titrated to cholesterol levels vs fixed-dose treatment

A

In secondary prevention (patients with coronary artery disease, target lipid of 50-70 mg/dL), it is NOT INFERIOR to fixed dose high-intensity statin

no evidence for primary prevention

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25
What do trials say for using low dose vs high dose statins in PRIMARY prevention?
no evidence to show advantage
26
JUPITER trial PICO primary/secondary
P: high sensitivity CRP patients (intermediate risk but high risk) -> have good LDL I: Rosuvastatin 20 (high dose) Primary prevention GOOD FOR PATIENTS WITH HIGH CR PROTEIN
27
What is the relationship between incidence of diabetes vs statin in both primary and secondary prevention
Slight increase in diabetes incidence - OR is 1.09 (overestimation) - 6% risk of diabetes with statin Overall: Ok to use statin since for every 1 patient that gets diabetes from statin, we save 11 from CVD
28
What are the 3 types of ADRs of statins HMG
H Hepatic effects M Muscular effects G Gastrointestinal effects
29
Is statin hepatotoxicity dose dependant? Solution? effect on patients with liver disease?
Yes dose dependant - inc hepatic transaminases Solution: reduce dose or change statin Statins actually improves fatty liver transaminase
30
How do we monitor statin hepatotoxicity? How often?
Measure ALT/AST at baseline - then at 12 weeks after starting therapy - then annually
31
Define Myalgia Myositis Rhabdomyolysis
Myalgia: - muscle pain/weakness with NO creatinine kinase CK elevation Myositis: - muscle symptoms with inc CK levels Rhabdomyolysis - muscle symptoms with HIGHLY INC CK levels (10x+ upper limit) - SCr elevation - urine may be brown due to existence myoglobin
32
What are risk factors for statin induced myopathy?
- Age 80+ - Female - LOW BMI - DM - Liver/renal dysfunction - Hypothyroidism untreated - Trauma/surgery/heavy exercise - Drugs (fibrates, CCB, cyclosporine, amiodarone) (CYP inhibitions) - Genetics
33
Is it recommended to get baseline CK?
No
34
When to monitor for muscle symptoms in statins? What to do if symptomatic?
6-12 weeks after starting - then at each follow-up visit If symptomatic obtain a CK measurement
35
How to manage myopathy steps?
1. Reduce statin dose 2. switch statin 3. Alternate day dosing statins (surrogate data suggests similar effects) 4. Non-statin alternatives 5. Coenzyme q10 supplementation (no evidence)
36
When should LDL be monitored?
For estimating risk at baseline - maybe for adherence NOT FOR LIPID EFFICACY
37
Time of administration for statins
HS: for short acting (lovastatin, simva, fluva) - surrogate outcomes not clinical Any time in day: does not matter for long-acting
38
When are statins considered "not tolerated"
After trying at least 2 agents
39
Which non-statin agents have evidence in primary prevention? (2)
1. Gemfibrozil (fibrate) 2. Cholestryamine (Bile acid resin)
40
Which non-statin agents have NO evidence in primary prevention? (4)
- Ezetimibe - Niacin - PCSK9 inhibitors - CETP inhibitors
41
Helsinki Heart study PICO
P: high cholesterol MEN with non-HDL cholesterol of 5.2+ I: Gemfibrozil 600mg po BID C: Placebo O: MI (fatal, non-fatal), Sudden cardiac death
42
What are the limitations to the Helsinki Heart study?
- Studied long time ago - only men - Different population, back then people had higher cholesterol, large % of smokers
43
What is the most common ADR with gemfibrozil?
LOTS of GI symptoms - Better to try "4 statins" before gemfibrozil
44
What are fibrates good for in primary prevention?
Reduce risk for pancreatitis but no change CVD events vs placebo
45
LRC-CPPT trial PICO
P: primary prevention for men with total cholesterol over 6.8 I: Cholestyramine C: placebo O: Non-fatal MI and CHD moderate improvement in composite outcomes, NO improvement in mortality
46
How to administer Cholestryamine
Suspension (water or juice), not in dry form - should not be sipped or held in mouth (can cause tooth discolouration, or enamel decay) - administer with meal - needs to be titrated up from low dose
47
Cholestyramine safety
68% within the first year had mod-severe GI side effects - lowered to 29% pre-entry
48
Ezetimibe MOA What is efficacy based on?
inhibits intestinal absorption of cholesterol - 20% reduction in LDL - Efficacy based on surrogate markers (LDL, carotid intima-media thickness
49
What does data show about carotid intima media thickness CIMT?
CIMT is shown to be a significant predictor of future CVD event - however, slow regression in CIMT due to drugs was not found to be associated CVD outcomes
50
IMPROVE-IT PICO
P: patients with an acute coronary syndrome within the previous 10 days (SECONDARY) I: Simva 40mg + ezetimibe 10mg C: Simva 40 O: MI + stroke (non-fatal) and CHD death
51
IMPROVE-IT Outcome
Improved composite outcomes and not mortality
52
IMPROVE-IT Limitations
Did not use a high intensity simva in secondary trial
53
Can we use ezetimibe in primary prevention? As monotherapy in secondary?
No
54
Niacin MOA of HDL, LDL, Lpa
inc HDL at lower doses Dec LDL at higher doses Dec Lpa
55
AIM-HIGH trial PICO
P: Patients with CVD and low HDL (SECONDARY) I: Simva (40-80) + ER niacin (2000mg/day) C: Simva 40-80 + placebo (100-200mg of niacin) O: nonfatal MI, schemic stroke, hospitilzaation for an ACS, revascularization, Death from CHD
56
AIM-HIGH trial Limitations
Stopped early due to increased ischemic stroke in treatment group. More use of 80mg simva in placebo, higher HDL than expected - showed no benefits vs placebo Increase in mortality? Laropiprant effect?
57
Niacin safety?
Concerns for: Increased infections, myopathy, BG, Hepatic issues, hypotension, nigricans - 80% experienced flushing, poorly tolerated - must titrate dose - may need to premedicate with ASA or ibuprofen before dose
58
When do we consider Niacin?
Considered VERY LAST LINE in high risk patients (familial hypercholesterolemia), who still have HIGH LDL despite being on max statin dose + ezetimibe/bile resin
59
MOA of PCSK9
Increases LDL receptors, lowers LDL antibodies
60
Which drugs are PCSK9 inhibitors?
Monoclonal antibodies - Evolocumab - Alirocumab - Inclisiran
61
FOURIER trial (evolocumab) Population Outcome Side effect?
Population: - with atherosclerotic CV disease (previous MI, stroke or PAD) (SECONDARY) - LDL 1.8 mmol/L or higher - On a statin Outcome: - reduced LDL levels as add-on, NO improvement in mortality Side effect - injection site reaction was most significant
62
ODYSSEY Outcomes trial (Alirocumab) Population Outcome
Population - ASCVD disease (SECONDARY) - LDL over 1.8 mmol/l - HIGH intensity statins Outcome - better composite outcomes, mortality slightly improved (but insignificant)
63
Evolocumab injection indications (3)
1. Homo/heterozygous and familial hypercholesterolemia (in addition to max tolerated statins + other meds) 2. Clinical atherosclerotic CVD (in addition to max tolerated statins + other meds) 3. Off label use: high risk patients (in addition to max tolerated statins + other meds)
64
Inclisiran trials Outcome assessed? Surrogate outcome?
Outcome assessed? % change in LDL Surrogate outcome? - 50% change in LDL Still ongoing
65
Evacetrapib ACCELERATE trial outcome? Available in Canada? Class?
Cholestyeryl ester transfer protein (CETP) inhibitors - Not available in canada - Does not work
66
Cholestyeryl ester transfer protein (CETP) inhibitors MOA
block the transfer of cholesterol to VLDLs and HDLs - less cholesterol in periphery
67
CLEAR trials PICO
Population: - high risk primary (reynorlds risk score over 30%, type I or II diabetes aged, coronary artery calcium) - statin-intolerant - mixture of primary and secondary I: bempedoic acid vs placebo
68
Which combination studies showed improvement
Statin + omega-3 fatty acids (icosapent ethyl)
69
Icosapent Ethyl PICO
Population - INCREASED Triglycerides 1.52-5.63 - on a statin (mod-high dose) - PRIMARY AND SECONDARY Significant in reducing clinical outcomes in patients with decent statin dose
70
When do we consider ezetimibe vs PCSK9 inhibitor
PCSK9 - LDL 2.2+ mmol/L - ApoB 0.8+ - non-HDL 2.9+ Ezetimibe - all lower

IPFC 3 Final (6 decks)

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