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Cardiology > Coronary artery disease > Flashcards

Coronary artery disease Flashcards

1
Q

Is there a proven mortality benefit in secondary prevention following ACS with high-intensity statin therapy, irrespective of pre-treatment LDL?

A

Yes

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2
Q

What are some side-effects of statin therapy?

A

True adverse effects over publicied and not proven in trials

Myalgias most common reason for cessation; not associated with CK rise or alteration on muscle biopsy
Rhabdomyolysis and myositis are very rare <0.5%
Hepatotoxicity very rare <0.1%

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3
Q

WSCOPS Trial

A

Showed mortality benefit in primary prevention with moderate intensity statin therapy for people with LDL>4.0mmol/L or those with 10-year CV risk >7.5%

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4
Q

FOURIER trial

A

Randomised, double-blind, placebo-controlled
N=27,500
Evolocumab vs Placebo
Inclusions: CAD and LDL > 1.8 and on statin therapy
Endpoint: 1’ Cardiovascular death, MI, stroke, hospitalisation for unstable angina, revascularisation
Median follow up 2.2 years
Mean percent reduction of LDL was 59%
Evolocumab (9.8%) vs. Placebo (11.3%) event rate (Hazard ratio 0.8, CI 0.73 - 0.88)

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5
Q

What was the EVOPACS study (2019)?

A

Compared evolocumab + statin to placebo + statin in ACS patients
N = 308
90% of evo + statin achieved LDL<1.4 vs. 10% with placebo + statin

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6
Q

What is the LDL-C lowering effect of PCSK9i + High-intensity statin + ezetimibe?

A

~85%

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7
Q

Name two PCSK9 inhibitors

A

Evolocumab and Alirocumab

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8
Q

What is the PCSK9 inhibitors MOA?

A

PCSK9 binds to LDL-receptor on the surface of hepatocytes resulting in internalisation of the receptor and reducing the number on the surface able to bind LDL.

Inhibiting PCSK9 more LDL-R remain available to bind serum LDL and removing them from circulation.

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9
Q

ODYSSEY Trial

A

Multicentre, randomised, double-blind, placebo controlled
N= ~19000
Inclusions: ACS 1 - 12 months prior and LDL at least 1.8mmol/L and on statin at maximal tolerated dose
End-points: 1’ Death by CAD, non-fatal MI, ischaemic stroke, unstable angina requiring hospitalisation
Follow up at 2.8 years (median)
Placebo (11.1%) vs. Alirocumab (9.5%): Hazard ratio 0.85 (CI 0.78 - 0.93)
** Benefit greatest amongst those with higher baseline LDL levels

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10
Q

What is the LDL-C lowering effect of PCSK9 inhibitor alone?

A

60%

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11
Q

What is the LDL-C lowering effect of PCSK9 inhibitor + high-intensity statin?

A

~75%

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12
Q

What is the LDL-C lowering effect of High-intensity statin?

A

~50%

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13
Q

What is the LDL-C lowering effect of high-intensity statin + ezetimibe?

A

~65%

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14
Q

When should you measure Apolipoprotein A levels? (5)

A
  • premature CVD or stroke
  • intermediate CVD group  if levels are elevated they go into higher risk group
  • recurrent or rapidly progressive vascular disease
  • Familial hypercholesterolaemia, genetic dyslipidaemia or low HDL-C
  • Elevated CVD risk
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15
Q

What is the average reduction in LDL cholesterol for patients taking Ezetimibe 10mg?

A

20%

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16
Q

How is Familial Hypercholesterolaemia diagnosed?

A

Dutch Lipid Clinic Network Criteria

Domains include; family history, clinical history, physical examination, biochemical results and genetic testing.

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17
Q

What are the cut-offs for Dutch Lipid Score to diagnosed Familial Hypercholesterolaemia?

A

0 - 2: unlikely
3-5: possible
6-8: probable
>8: definite

18
Q

How do you treat elevated Lipoprotein A levels? (5)

A
  1. Aggressive LDL reduction (<1.5mmol/L)
  2. ACEi in proteinuric patients
  3. Nicotinic acid
  4. LDL-apheresis
  5. Anti-Lp(a) antisense and other novel therapies (PSCK9-I, mipomersen, CETP)
19
Q

What do evolocumab and alirocumab target?

A

PCSK9-inhibitor

20
Q

What is Apolipoprotein A

A

LDL-like particle with apolipoprotein A bound covalently to the surface

21
Q

What clinical signs are associated with familial hypercholesterolaemia?

A

Cholesterol accumulation in tendons (achilles tendon), arcus lipoides

22
Q

What is the mode of inheritance for Familial Hypercholesterolaemia?

A

Autosomal dominant

23
Q

What percentage of patients with definite Familial Hypercholesterolaemia do not have an identifiable mutation?

A

20%

24
Q

What is the incidence of familial hypercholesterolaemia? (in Australia)

A

1/250

25
Q

ORBITA trial

A

Showed that real PCI did not improve outcomes in stable CAD compared to sham PCI

26
Q

FAME study

A

Showed FFR<0.8 as significant flow limitation

27
Q

ASPREE trial

A

No role for aspirin in primary prevention of CVD who are low-intermediate risk who are asymptomatic

28
Q

DEFER study

A

Showed FFR <0.75 as significant flow limitation

29
Q

What is the goal waist circumference in men and women?

A

M <102cm and F<89cm

30
Q

PROMISE trial

A

CTCA to investigate chest pain did not improve mortality or CVD outcomes, but did result in more “positive” angiograms

31
Q

Is FFR validated in ACS cohorts?

A

No, only stable CAD

32
Q

What is the management for stable coronary artery disease?

A
  1. Antiplatelet (aspirin or clopidogrel)
  2. Statin
  3. B-blockers
  4. Treat risk factors
  5. Angiography reserved for severe or unstable angina despite optimal medical therapy, large burden of ischaemia on stress testing or ACS
33
Q

What percentage of patients with acute myocardial infarction have chest wall tenderness?

A

~15%

34
Q

COURAGE trial

A

medical therapy outweighs the benefits of PCI in stable CAD

35
Q

What factors are associated with increased likelihood of atypical presentation of ACS?

A

The elderly, female, diabetics.

36
Q

Grading angina

A

Canadian cardiovascular society score

  1. Angina only with strenuous exertion (onset with strenuous, rapid or prolonged ordinary activity)
  2. Angina with moderate exertion (slight limitation of ordinary activities when performed rapidly, after meals, in cold, in wind or under emotional stress)
  3. Angina with mild exertion (difficulty walking 1-2 blocks, climbing stairs)
  4. Angina at rest (no exertion needed)
37
Q

Risk factors for coronary artery disease

A 
Age
Gender
Smoking status
Diabetes
Hypertension
Cholesterol
ATSI status
38
Q

What do “high”, “intermediate” and “low” cardiovascular risk mean?

A

High risk: >15% annual risk of death, stroke or MI
Intermediate: 10-15%
Low: <10%

39
Q

Define typical angina

A

all three of the following must be met:

  1. constricting discomfort in chest, neck, shoulder, arm or jaw
  2. precipitated by physical exertion
  3. relieved by rest or nitrates within 5 minutes
40
Q

What percentage of ACS patients have sharp or pleuritic pain?

A

5-19%

41
Q

What is the goal BMI?

A

18.5 to 24.9

Cardiology (21 decks)

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