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Cardiovascular Therapeutics > Cholesterol Tx > Flashcards

Cholesterol Tx Flashcards

1
Q

Statins are a….

A

HMG-CoA reductase inhibitors

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2
Q

Statins main effect is on…..

A

LDL levels in the blood

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3
Q

Statin Examples

A

Atorvastatin
Fluvastatin
Lovastatin
Pravastatin
Rosuvastatin
Simvastatin

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4
Q

Statin MOA

A

Inhibits an enzyme in the pathway for intracellular synthesis of cholesterol

Cellular levels of cholesterol become depleted

Cell upregulates LDL receptor

LDL levels in the blood decrease

Primary site of action appears to be hepatic cells  liver takes up a bunch of LDL

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5
Q

Statins primary Site of ACtion

A

Liver - Hepatocytes

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6
Q

Statin Benfits

A

Clinical benefits of LDL lowering have been demonstrated repeatedly

Similar to HTN control, lipid reduction is NOT a cure for ACVD

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7
Q

The most benefit of statins in….

A

Greatest absolute benefit occurs in patients with a “statin-indicated condition” due to their high global risk

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8
Q

greater benefits are a reesult of

A

Greater LDL reductions

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9
Q

Current Strategy of Statin Usage. Why?

A

Maximize statin dose in everyone who can tolerate it

Trials show that high dose statins are better than low dose statins

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10
Q

Statin effects on other plasma proteins. Are we certain?

A

HDL may ↑ 5-10% (up to 15% or not at all)

TG ↓ up to 30% (higher baseline TG = greater effect)

Benefits of these effects UNCLEAR

LDL - Can be lowered up to 50%

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11
Q

What is the most controversial aspect of statin tx?

A

One of the MOST controversial aspects of statin therapy is its role in LOW risk patients

Primary prevention

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12
Q

When is benefit of a drug reduced?

A

If few events are occurring WITHOUT drug, the opportunity for benefit is drastically reduced

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13
Q

NNT in Statin Tx that is acceptable

A

NNT of <50 to prevent 1 CV event over 5 years is generally accepted as reasonable for statins (threshold for where they think statins are of benefit)

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14
Q

Are the benefits of statins the same for everyone?

A

For statins, relative benefits seem to be the same in everyone assuming a fixed LDL reduction.

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15
Q

The NNT is often impcated by….

A

Thus, NNT is generally impacted by the RISK level

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16
Q

The recommended use of statins is based on…

A

RISK

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17
Q

Why can’t diets/lifestyle be used to reduce LDL?

A

Diets are terrible at lowering LDL levels

Healthy Lifestyles –> Start way to late –> If you are 60, this is nieve –> Do not have time to change their life as much as a 20 year old

Critical for global CV risk reduction

Limited benefits for LDL specifically

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18
Q

Risk of early onset of dz is reduced when…

A

Healthy diet/lifestyle throughout life would almost eliminate an individual’s risk (at least for early onset dz)

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19
Q

Is titration needed with statin meds?

A

NO

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20
Q

High Intesnity Statin Lowers LDL by…. Examples

A

> than or equal to 50%

Atorvastatin 40/80 mg
Rousuvastatin 20/40

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21
Q

Moderate Intensity Statins Lower LDL by…. Examples

A

30-49%

Atorvastatin 10-20mg
Rousuvatstain 5-10mg
Simvastatin 20-40 mg
Pravastatin 40-80 mg
Lovastatin 40-80 mg
FLuvastatin 40 mg

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22
Q

Low intensity Stains lower LDL by… Examples

A

<30%

Simvastatin 5-10mg
Pravustatin 10-20 mg
Lovastatin 10-20 mg

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23
Q

Why do all pt’s get high-dose statins?

A

More intensive LDL reduction is clearly associated with greater protection against ACVD events

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24
Q

Exceptions to high dose strategy?

A

Intolerance
Drug interactions
Patient preference

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25
Time to effect STATINS
Time – wait at least 6-12 weeks to ensure full effect
26
Statin Time to Effect
6-12 weeks
27
Chart for Intensifying tx
28
Statin Indicated COndition and TX
29
Artherosclerosis Intensification
30
PCSK9
Evolocumab Alirocumab New and expensive
31
PCSk9 MOA
PCSK is An enzyme that promotes degradation of the LDL receptor on hepatocytes. (antibodies to the enzyme) Alirocumab and evolucumab are antibodies to PCSK9 Fully “humanized” monoclonal antibodies Result is increased expression of LDL receptors on hepatocytes and increased clearance of LDL from blood
32
Are PCSK9 safe to use with statins?
Yes --> Different mechanism
33
PCSk9 Criteria
40 to 85 years of age Clinically evident atherosclerotic disease MI Ischemic stroke PAD LDL 1.8mmol/L or higher (or Non-HDL at least 2.6mmol/L) Currently taking Atorvastatin equivalent of 20mg/day (why on 20 is b/c most likely could not tolerate the high dose)
34
Ezetimibe MOA
Inhibits luminal cholesterol absorption in small intestine ↓ cholesterol absorption = ↓ chylomicron formation ↓ chylomicron remnants to the liver = ↓ hepatocyte chol ↑ LDL receptor expression in liver = greater clearance of LDL LDL reduces LDL by 15% to 20% as monotherapy (weak)
35
Ezetimibe undergoes....
Despite its local effect, the drug undergoes enterohepatic recirculation
36
Is ezetimibe used in monotx?
No
37
Ezetimibe is combined with statins when.....
Statin escalation impossible – tolerability --> Use Atorvo 20 and add ezetimibe can equal high does statin LDL reduction Statin dose maxed out – LDL still not at goal
38
Eicosapent Ethyl
Eicosapent Ethyl (n-3 fatty acid)  Omega-3 fatty acids Purified ester of EPA (eicosapentaenoic acid) (fish source)  Now in guidelines  NOT AN LDL DRUG
39
Inclisiran
interferes with PCSK9 messenger RNA
40
Bempedoic Acid
Inhibitor of ATP citrate lyase – reduced cholesterol synthesis
41
Stain Tolerability Variability
Very Variable
42
Statin S/e
GI discomfort Fatigue Rhabdomyolyisis --> Rare Muscle effects  Rhabdomyolysis (ultimate neg muscle outcome)  such inflamed muscles, muscles rupturing and letting go of myoglobin Diabetes (increased detection) --> VERY LOW --> Increase blood glucose Cognitive Impairemnt - Low
43
Myopathy
Muscle Pain
44
Myalgia
CK < or eqaul to ULN
45
Myositis
CK > ULN
46
Rhabdomyolysis
CK > 10 times ULN
47
CK Tests ULN
Creatinine Kinase Tests Upper Limit of Normal
48
When are CK tests ordered?
Ask about muscle diseases, wasting/frailty  may indicate higher risk for statin-myopathy (might consider lowering statin dose) If the risk for muscle effects is high, consider a baseline CK (i.e., before statin started) Otherwise, CK levels ONLY ordered if symptoms appear
49
To ensure muscle sx are from statin?
Ensure it is from the statin Symptoms resolve when statin d/c Symptoms recur when statin restarted Symptoms recur when another statin tried
50
How to deal with intolerability?
D/c statin for short period, re-challenge after resolution of symptoms Lower doses / every other day dosing Lower potency statins (e.g., fluvastatin) Non-statin drugs
51
Most likley origin of DI's for statins
Hepatic Metabolism
52
All statins undergo the
First Pass effect
53
All statins are metabolized by...
Liver
54
Interactions of Statins
3A4 / grapefruit juice
55
C.I. of Statins
People with muscle disease Gemfibrozil (fibrates can increase adverse muscular effects)
56
Dosing of Statins
OD
57
Which has fewer drug interactions?
Rosuvastatin – fewer drug interactions vs atorva
58
In renal disease, use this statin?
Atorvostatin Reduce dose if CrCl <30m/min for ROSUVA ---- Atorva does NOT require dose adjustment in renal dysfx
59
Family HX
Family history – First degree relative with established ASVD at young age (<55 males/<65 females)
60
Lp(a)
Lp(a) – an LDL molecule covalently bonded to an Apo A. Highly genetic predisposition that is associated with higher risk
61
CAC
Coronary Artery Calcium. An imaging test that can reveal how much disease activity is (was) present in the coronary arteries. High CAC indicates higher risk.
62
LDL Lowering Effect
LDL lowering will always produce lower outcome rates As LDL reaches low levels CV benefits are smaller with additional LDL lowering
63
LDL Loweri g Add-On Effecr
LDL lowering much greater with PCSK9
64
What agent to add when TG's are elevated?
Icosapent EThyl
65
Risk of High TG's
Pose a CV risk – However, no proven drugs to reduce CV risk until IPE Very high TG’s = 14% risk of pancreatitis (a non-CV outcome) --> MAJOR --> Enzymes breakdown pancretic tissue and leak into abdomen
66
Main cocnern with high triglycerides
PANCREATITIS
67
Blood tests - TG's
Blood tests measure “triglycerides” rather than VLDL and chylomicrons separately TG blood tests measure all TG levels in the blood (VLDL + Chylomicrons)
68
High TG's and Tx Considerations
69
Major Contributors to high TG's
70
Drugs Increasing TG's
71
Drugs used for lowering TG's and its effect
72
Niacin Effect on TG's and LDL
TG Dceraese 27% (1.9 --> 1.4) after 2 yrs Nothing for CV
73
Fenofibrate TG and CV Effect
Lowered TG by 27% Higher rate of death due to CHD (CHANCE)
74
Omega-3 Fatty ACids TG's
EPA and DHA - 2 predominant n-3 fatty acids in fish and omega-3 supplements Many non-prescription omega-3 fatty acids available. Can lower TG’s when the dose of EPA+DHA = 2-4g per day. Efficacy similar to fibrates (30%-50% lowering).
75
Omega-3 Effect on TG's
Simialr to FIbrates
76
Summary of Elevated TG and TX
77
What is icosapent ethyl
78
Risk ENhancing Factors CV Guidleines
79
Lp(a) Defintion
80
CAC Defintion
81
hsCRP Defintion

Cardiovascular Therapeutics (5 decks)

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