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344 > Dyslipidemia Tx Options - Statins > Flashcards

Dyslipidemia Tx Options - Statins Flashcards

1
Q

Health Behaviour Modifications

• Recommend for all patients at risk of CVD

A
  • Smoking cessation
  • Single most important health behaviour intervention for CVD prevention
  • Dietary – it is recommended that all individuals adopt a health dietary pattern
  • dietary modifications: calorie restriction, dietary fibre intake of >30 g daily, substitute unsaturated fats for saturated/trans fats, fruits and vegetables, limit cholesterol intake
  • referral to dietician/nutritionist, where appropriate
  • Exercise – it is recommended adults accumulate 150 mins/week of moderate to vigorous intensity aerobic physical activity
  • Limit EtOH intake ‐‐ limit to 1‐2 drinks per day
  • Psychological stress management
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2
Q

Pharmacologic Treatment

A
  • HMG-CoA reductase inhibitors (statins)
  • Cholesterol absorption inhibitor (ezetimibe)
  • Niacin
  • Fibrates
  • Bile acid sequestrants (BAS)
  • PCSK9(Proprotein Convertase Subtilisin/Kexin type 9) inhibitors
  • Icosapent ethyl (IPE)
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3
Q

Relative Effects of Different Agents

see slide 45 for more

A 
Statins 
LDL-D decrease 30‐50%
(agent and dose dependent)
HDL-C dec 4‐10% TG dec 20‐30%
(>effect with higher TG)

Ezetimibe LDL-C dec 15‐20%
PCSK9‐i LDL-C dec 50‐60%

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4
Q

Statins – Mechanism of Action (MOA)
• Statins are the cornerstone of dyslipidemia management ‐‐ recommended as the initial lipid‐lowering agent of choice for treatment.
• Maximum dose or maximally tolerated statin should be used for all patients in whom treatment is indicated.

A
  • upregulation of LDL‐receptors
  • causes increased removal and catabolism of LDL‐C
  • decreased VLDL production (VLDL carries serum TG’s)
  • Promotes conversion of VLDL to LDL‐C
  • these mechanisms lead to reduction in TC, LDL‐C and TG’s
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5
Q 
Comparison of Statin LDL Lowering 
Rosuvastatin \_\_\_\_\_\_\_\_\_
Atorvastatin\_\_\_\_\_\_
Simvastatin 35 – 50
Lovastatin 25 – 40
Pravastatin 20 – 35
Fluvastatin \_\_\_\_\_\_

what are the doses for high intensity doses?

A

40 – 65
35 – 60
20-35

Everything except for rosu and ator is limited to moderate intensity reduction

ator: 40‐80 mg
rosu: 20‐40 mg

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6
Q

Statins LDL Lowering Effects

A

The law of diminishing returns

♥ “Rule of Sixes”: double dose = 6% LDL‐C lowering

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7
Q

Contraindications for statins

A
  • Active liver disease
  • Includes unexplained persistent elevations in ALT or AST and non‐alcoholic steatohepatitis (NASH)
  • Use low dose in chronic stable liver disease
  • No guidelines for dose reduction
  • Monitor more frequently for adverse effects
  • Pregnancy and lactation
  • Hypersensitivity
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8
Q

Statin Clinical Pearls
timing of dosing

why we Do not recommend simvastatin 80 mg daily – previously marketed dose?

• Pravastatin only statin not metabolized by ________

A
  • Less potent: take with evening meal or at hs
  • Atorvastatin and rosuvastatin: take any time
  • Atorvastatin and Rosuvastatin are the most potent statin, only ones that are truly high‐intensity

simvastatin
• No benefit over 40 mg daily
• Increased risk of myopathy

• Pravastatin only statin not metabolized by Cytochrome P450 enzymes
– useful when concerned about serious/significant drug interactions

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9
Q

statin metabolism

A 
Atorvastatin CYP3A4
Fluvastatin CYP2C9
Lovastatin CYP3A4
Pravastatin Not well understood (not CYP)
Rosuvastatin CYP2C9
Simvastatin CYP3A4

• Mnemonic for CYP3A4 statins: A.L.S.

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10
Q

what increases statin levels by interacting with CYP34A inhibitors

A
  • Macrolide antibiotics (e.g., clarithromycin)
  • Grapefruit juice
  • Azole antifungals
  • Protease inhibitors
  • Other drugs that may decrease statin metabolism: amiodarone, diltiazem, verapamil, cyclosporine/tacrolimus, ± amlodipine
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11
Q

Decrease Statin Levels

A
  • Rifampin
  • Carbamazepine
  • Phenytoin
  • Bosentan
  • Efavirenz
  • Antacids
  • Rosuvastatin + magnesium/aluminum antacids
  • Dose antacid 2 hr after rosuvastatin
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12
Q

Approach to Drug Interactions

A
  • Assess level of risk based on interaction, patient, situation
  • If low risk, no additional monitoring required
  • If high risk, consider alternative
  • If no alternative exists, consider duration of therapy
  • If duration ≥10 days, consider reducing dose/monitoring
  • Caution in specialty populations
  • Solid organ transplant (SOT) recipients and patients with HIV
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13
Q

Adverse Effects

A
  • “Generally well tolerated” by the great majority of patients
  • GI: nausea/vomiting/diarrhea
  • MSK: myopathy
  • HEPATIC: elevated liver enzymes
  • ENDO: diabetes –in those predisposed (IFG, IGT, or prediabetes)
  • Multiple rare adverse effects (<1%)
  • “Nocebo effect”: people who have negative expectations about medicine or a treatment experience harmful symptoms they otherwise wouldn’t have.
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14
Q

describe the Statin Nocebo Effect

A

“Nocebo effect”: A situation in which a patient develops side effects or symptoms that can occur with a drug or other therapy just because the patient believes they may occur.
• people who have negative expectations about statins may experience symptoms of side effects that they otherwise wouldn’t have.
• opposite of a placebo effect

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15
Q

muscle‐related pathology
muscle pain with CK ≤ ULN
myalgia with CK > ULN

muscle breakdown with CK >10x ULN ± serum myoglobin and renal failure

A

• Creatine kinase (CK): tissue enzyme (particularly in
skeletal muscle) that is released during muscle
breakdown

mypoathy
myalgia
myositis
Rhabdomyolysis

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16
Q

Myopathy from statin

A
  • Incidence: 1.5 – 5%
  • Class effect
  • Possibly dose‐related
  • Usually occurs in first 6 months of therapy
  • Does not require CK elevation (myalgia)
  • Pain usually presents in large muscle groups
  • ≥40% of patients will tolerate another statin
17
Q

Risk Factors for Myopathy

A
  • Hx of myalgias with statins
  • Hx of unexplained muscle aches or positive FamHx
  • Hypothyroidism
  • Renal or hepatic impairment
  • Female
  • Small body frame
  • Advanced age
  • Drug interactions
18
Q

Rhabdomyolysis

A

Incidence 0.04% (1 in 2,500 patients)
• Myoglobinemia  myoglobinuria
• Can lead to acute renal failure (darkens urine)
• Not well predicted by myalgias
• Likely dose‐related
• Increased risk with fibrate combination
• Discontinue statin and do not rechallenge

19
Q

Approach to Monitoring for myopathy

A
  • Baseline CK and TSH in all patients
  • Asymptomatic  no routine CK monitoring
  • CK elevated by exercise, trauma, infection
  • Symptomatic  d/c statin and measure CK
  • CK ≤ ULN  reassess symptoms and CK in 6‐12 weeks
  • Resume statin once patient asymptomati
  • CK <10x ULN  consider other causes, follow until CK ≤ ULN and patient asymptomatic, then restart different statin or lower dose
  • CK >10x ULN  hydrate PRN, follow until CK ≤ ULN and patient asymptomatic, then restart different statin or lower dose (if moderate to severe, consider alternate therapy)
  • Muscle biopsies have no role – low diagnostic yieldc
20
Q

Coenzyme Q10

A

• Meta‐analysis of 6 RCTs (N = 302) showed no effect on muscle pain or
CK in patients on statin therapy
• Not recommended as per CCS guidelines
• No known risks of coenzyme Q10
• Patients that have a perceived effect (placebo) should not be dissuaded

21
Q

Statin‐Induced Liver Enzyme Elevation

A
  • Incidence: 0.1 – 3%
  • Most often will present with ALT elevation
  • More specific to liver vs AST
  • Generally asymptomatic
  • Usually occurs in first 6 months of therapy
  • May be dose‐related
  • Does not predict liver damage or failure
  • 1 in 1.14 million
22
Q

Approach to Monitoring Liver Enzyme Elevation

what are some signs and symptoms?

A
  • Baseline ALT
  • Check ALT at 6‐12 wk post‐statin initiation
  • If ≤3x ULN, no routine ALT monitoring required
  • If >3x ULN, d/c statin and reassess in 6‐12 wk
  • If persistently >3x ULN  investigate etiology
  • If ≤3x ULN, restart at lower dose or switch statin and reassess in 3‐6 wk
  • Asymptomatic elevation in ALT may return to normal with continuation of statin, dose reduction or discontinue
  • Monitor for signs and symptoms of liver failure
  • Jaundice, fever, malaise, lethargy, dark‐coloured urine, or abdominal pain
  • If occur, d/c statin and seek medical attention
23
Q

New Statin Safety Concerns

A
  • Diabetes: associated with small increased risk but benefits outweigh risk. Statins only unmask diabetes in patients at risk (IFG, IGT, or prediabetes)
  • Cancer: no association and may actually improve survival in some populations
  • Cognition: no association with cognitive decline; rare adverse effect
  • Fatigue: poor quality evidence
  • Cataracts: small association in retrospective cohort data
24
Q

Statin Adherence
what did the Ontario Cohort Study show?

Tips to Improve Adherence

A 
Adherence rate to statins
over 2 yr:
• Recent ACS: 40.1%
• Chronic CAD: 36.1%
• Primary prevention: 25.4%
  • Educate patient emphasizing benefits
  • Challenge in preventative therapy
  • Demystify concerns over harm
  • Address patient‐specific concerns
  • Simplify regimen
  • Adherence aids
  • Contact and follow‐up

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