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FRACP > Cardiology > Flashcards

Cardiology Flashcards

1
Q

True/False: low dose rivaroxaban decreases mortality in ACS?

A

True.

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2
Q

Which is better at preventing stroke and systemic embolism in non-valvular AF - warfarin or apixiban?

A

Apixiban:

  • Lower rates of ICH
  • GI-bleed and MI are equivalent between the 2 groups.
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3
Q

What is a common SE of ticagrelor?

A

SOB

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4
Q

What percentage of HF has preserved EF?

A

40-60% of heart failure is HFpEF.

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5
Q

What is Beck’s triad? (clinical utility and features)

A

Suggestive of acute cardiac tamponade (HHH):

  1. High JVP
  2. HS hard to hear
  3. Hypostension
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6
Q

What deleterious effect upon the ECG has methadone?

A

Prolongation of QTc

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7
Q

True/False: statin reduces all-cause mortality as primary prevention in hypercholesterolaemia.

A

True.

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8
Q

What is the MOST important consideration in the evaluation of a patient with any type of valvular disease when considering valvular intervention.

A

Symptoms.

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9
Q

What are mean gradient (mmHg) echo criteria for severe disease in:

  1. AS
  2. MS
  3. TS
A
  1. AS > 40
  2. MS > 10
  3. TS > 5
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10
Q

What is the echo criteria for severe AS (multiple of 4s) - give the full complement.

A

Velocity ratio < 0.25
Valve area < 1.0 cm^2
Maximum jet velocity > 4 m/s
Mean gradient > 40 mmHg

Multiples of 4s:
0.25 / 1.0 / 4 / 40
VR / VA / mJV / mG

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11
Q

What valve area size on echo suggests severe AS or MS?

A

< 1.0 cm^2

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12
Q

True/False: an angiogram should be considered prior to all valve procedures.

A

True.

Level 1C recommendation/evidence:
o Angiogram should be conducted prior to valve surgery to look for CAD.
o Secondary MR is usually due to ischaemia
o CABG for lesions >70% at time of valve surgery

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13
Q

What is the post-op mortality of valve repair for AV and MV?

A

AVR / no CABG = 3%
AVR + CABG = 6%
MVR / no CABG = 4%
MVR + CABG = 8%

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14
Q

What four conditions would prompt endocarditis prophylaxis periprocedurally?

A

Current recommendations:

  1. prosthetic valves
  2. previous endocarditis
  3. cyanotic congenital heart disease
  4. high risk lesions e.g. PDA
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15
Q

What is the endocarditis prophylaxis regimen for rheumatic fever?

A

Post-rheumatic fever exposure: daily penicillin for at least 10 years or until age 40 years (whichever is LONGEST) - remember 10/40.

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16
Q

If a patient is less than 50 yrs what is the most likely cause of AS?

A

Bicuspid AV.

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17
Q

If a patient is greater than 65 yrs what is the most likely cause of AS?

A

Calcified AV.

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18
Q

What is the impact of the presence of symptoms on the prognosis of severe AS?

A

Asymptomatic (may need EST to confirm) = < 1% annual death rate.

Symptomatic has < 50% five year survival rate, therefore intervention is recommended if patient is suitable.

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19
Q

True/False. Age is a contraindication for AS surgery (i.e. >80 yrs)

A

False.

Mortality rates: 1% for 80yrs

Post-Sx ‘older’ patients have similar life expectancy to age-matched controls (i.e. already old).

Post-Sx ‘younger’ patients have slightly worse life expectancy that age-matched controls.

Conclusion: surgery will still benefit px of 80yrs therefore age is NOT a contraindication.

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20
Q

True/False. AV valvuloplasty is more useful in adults than children for severe AS.

A

False.

Valvuloplasty for AS:

o Good for children but only short-term benefit for adults (weeks to months).

o Utility of valvuloplasty in adults is to ‘buy time’ e.g. pregnant woman with severe AS, reduce anaesthetic risk of non-cardiac surgery in older patients.

o Determine symptomatic benefit prior to definitive surgery in high-risk surgical patients with an alternative cause of symptoms e.g. intercurrent severe COPD.

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21
Q

What are 4 indications for AVR (Class 1 recommendation)?

A
  1. Severe AS and any symptoms related to the AS
  2. Asymptomatic severe AS with EST that elicits AS-related symptoms i.e. pre-symptomatic
  3. Severe AS undergoing CABG / ascending aorta / other valve
  4. Severe AS and LV dysfunction (EF<50%) not due to another cause

Summary:

Severe AS with symptoms (+/- EST) / need for cardiac Sx / LV-dysfunction

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22
Q

What is the 30d mortality of TAVI?

A

10% (i.e. not low)

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23
Q

What 2 therapeutic options do patients with contraindications to AVR have? What guides your choice between these options?

A

If life-expectancy < 1yr = medical mx (palliative)

If life-expectance > 1yr = TAVI

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24
Q

Patient with severe AS is asymptomatic but has LVEF < 50%, what is recommended?

A

AVR

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25
Q

True/False: most people with severe AS will need AVR.

A

True. Few exceptions (life expectancy and high surgical risk)

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26
Q

Paitent with severe AS has life-expectancy of <1yr - should a TAVI be offered?

A

No.

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27
Q

Give 5 absolute contraindications to TAVI for severe AS that are anatomical.

A
  1. Annulus size (less than 18 or greater than 29 mm^2)
  2. LV thombus or plaque/thrombus in ascending aorta/arch
  3. Endocarditis
  4. Coronary ostium obstruction risk
  5. Vascular access difficult
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28
Q

Assuming patient was suitable for a TAVI, is the 5 year follow-up prognosis better than medical therapy for symptomatic severe AS.

A

Yes.

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29
Q

With continuous doppler studies what direction of flow is above the line vs below the line.

A

“Down and out!”

Above the line = retrograde flow.

Below the line = anterograde flow.

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30
Q

What 2 conditions cause acute severe AR?

A

Aortic dissection or endocarditis.

Requires emergency surgery.

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31
Q

Give 5 causes of chronic AR.

A

HM-BED (her majesty’s bed):

  1. HTN
  2. Marfan’s
  3. Bicuspid AV
  4. Endocarditis (previous)
  5. Degenerative (often with AS).
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32
Q

What is the mortality of chronic severe ‘symptomatic’ AR without intervention?

A

20% (high)

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33
Q

What is the mortality of chronic severe ‘asymptomatic’ AR with LV-dysfunction without intervention?

A

20% (high)

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34
Q

True/False: AR is best remedied with repair rather than surgery (i.e. AVR).

A

False.

AR almost always requires AV replacement, repair is possible but not as durable as MV repair and may require re-operation within a few years.

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35
Q

Comment on the type of anticoagulation required for:

  1. Bioprosthetic valves
  2. Mechanical valves
A

Bioprosthetic valve = warfarin not required
Mechanical valve = warfarin required

NOACs are CONTRAINDICATED post-valve replacement

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36
Q

When is surgical AVR indicated in severe AR (3)?

A
  1. Symptomatic severe AR
  2. Asymptomatic severe AR with:
    a. LVEF < 50% or LV dilatation
    b. Need for other cardiac Sx
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37
Q

What are the indications for aortic root surgery? What severity of AR would trigger concern?

A

Aortic root surgery indicated (regardless of AR severity) if size of aortic root:

  1. > 55mm - anyone
  2. > 50mm - Marfan’s or Biscuspid with risk (FHx of rupture)
  3. > 45mm Marfan’s with risk (FHx of rupture)
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38
Q

What is the medical therapy for aortic root/arch disease?

A

Beta-blocker slow down aortic dilatation

ARBs (Candesartan) may preserve Elastin

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39
Q

When is TTE screening indicated in aortic root/arch disease?

A

• TTE screening of first-degree relatives in Marfans or Bicuspid patients with dilated aortic root (i.e. >50mm)

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40
Q

What are the causes of mitral stenosis, which is most common (3)?

A
  • Mostly rheumatic fever
  • Occasionally mediastinal radiotherapy
  • Rarely calcified/degenerative
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41
Q

True/False: Balloon valvuloplasty of the MV is more durable than AV valvuloplasty.

A

True.

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42
Q

Patient has moderate MR and symptomatic MS, which is preferable balloon valvuloplasty or surgical MVR?

A

Surgical MVR.

Anything more than ‘mild’ MR cannot have valvuloplasty.

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43
Q

Give 6 contraindications of MV valvuloplasty/PMC (percutaneous mitral commisurotomy) that would mean that a patient would need surgical MVR (seperate into MV-related and non MV-related).

A

MV-related:

  1. Valve area > 1.5cm^2
  2. > Mild MR
  3. Commissure abnormalities (severe bicommissural calcification or absence of commissural fusion)
Not related to MV: 
1. Left atrial thrombus
2. Concomitant 'severe' AS / AR / TR / TS
3. Concomitant CAD requiring CABG
NB: suggest need for Sx anyway
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44
Q

Whish is preferable in the treatment of severe mitral stenosis: valvuloplasty or MVR?

A

Valvuloplasty.

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45
Q

Which scenarios of MS require anticoagulation with warfarin vs. aspirin? What is the INR target?

A

MS – anticoagulation:

o Warfarin only (with higher INR 2.5-3.5):
• MS + AF (not NOAC)
• MS + SR + previous embolism
• MS + SR + LA thrombus or SEC (spontaneous echo contrast) on TOE
• Mechanical MVR

o Exception: Bioprosthetic MVR may use aspirin if LOW risk of AF, otherwise warfarin too!

Summary: Pretty much warfarin (not NOAC) for most scenarios and aspirin if bioprosthetic.

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46
Q

What is Barlow Syndrome?

A

Post-MI mitral prolapse due to papillary muscle rupture.

Requires TOE +/- invasive right-heart catheter for diagnosis (clinical signs and TTE unreliable as may miss jet) – giant v-wave.

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47
Q

What is the management of chronic severe MR:

  1. Asymptomatic
  2. Symptomatic
A
  1. MV-repair is often durable

2. MVR, severe LV-dysfunction confers poor prognosis.

48
Q

What is the difference between primary and secondary MR?

A

Primary MR: intrinsic problem with the chordae or leaflets e.g. rheumatic endocarditis, prolapse, flail.

Secondary MR: functional MR where valve is fine but the subvalvular apparatus are distorted e.g. LV dilatation from DCM, MI or LA enlargement.

49
Q

With MVR for severe MR, which type of MR confers worse survival post-op primary or secondary MR?

A

Surgical outcomes and longterm survival are worse in ‘secondary’ MR due to underlying pathology causing MR.

50
Q

Is the treatment for asymptomatic severe primary MR straightforward?

A

No - controversial.

MV repair may be considered if:

  1. LV dysfunction
  2. Severe pulmonary HTN +/- AF
  3. Large flail leaflet
51
Q

What is a 1C recommendation for ‘surgical’ MVR in chronic secondary MR?

A

Severe MR needing a CABG anyway.

52
Q

True/False: TR is almost always secondary and rarely needs intervention.

A

True - repair and replacement rarely required, fix pathology causing TR (e.g. pulmonary HTN)

53
Q

What are 3 causes of TS?

A
  1. Rheumatic fever
  2. Carcinoid
  3. Radiotherapy
54
Q

Is TS well-tolerated? What does it present with?

A

No - presents with RHF.

55
Q

When is tricuspid valve surgery indicated?

A
  1. For all symptomatic patients with severe TS
  2. Severe TS/TR undergoing left-heart valve interventions
  3. Symptomatic severe isolated primary TR without severe RV-dysfunction
56
Q

True/False: patient desire is an important consideration when choosing between metallic and bioprosthetic valves.

A

True.

57
Q

True/False: Severe AS often becomes symptomatic in pregnancy.

A

Severe MS often becomes symptomatic during pregnancy, treat with bed rest, beta-blockers and consider valvuloplasty after 20 weeks.

Severe AS is not common in pregnant women, usually well tolerated with truly asymptomatic pre-pregnancy, consider valvuloplasty if deteriorates.

58
Q

True/False. Chronic AR and MR is well tolerated provided that LV function is preserved.

A

True.

59
Q

What are 3 considerations when choosing mechanical vs. bioprosthetic valves.

A

Choice of mechanical vs. bioprosthetic valve depends on:

o Patient preference
o Anticoagulation
o Expected longevity of valve vs. patient

60
Q

True/False: Amiodarone can cause anaemia and thrombocytopenia.

A

True.

Amiodarone may cause haemolytic or aplastic anaemia and/or thrombocytopenia.

61
Q

What is the MOA of Ezetimibe?

A

Decreases cholesterol absorption in the small intestines.

Second-line therapy and often used in conjunction with a statin.

62
Q

What is the effect of nicotinic acid on prothrombin time and platelet count.

A

Nicotinic acid (niacin or vit B3) is on of the essential vitamins (i.e. cannot be synthesised).

Increased PT and decreased platelets.

63
Q

Which part of the lipid profile does nicotinic acid assist with in dyslipidaemia? Does it reduce mortality?

A

Increases HDL.

Unclear at present if it reduced mortality.

64
Q

In patients with HF what are 2 common comorbidities?

A

OSA and Depression

65
Q

In the pharmacotherapy of HF, list 6 medications, which of these actually improve mortality?

A

ABS-DAD:

Improve mortality:
ACEi/ARB
Betablockers
Spironolactone

More for symptoms:
Diuretics
Amlodipine
Digoxin

66
Q

List 3 cardio-selective beta-blockers.

A

Metoprolol SR
Bisoprolol
Carvedilol

67
Q

What is Epleronon and when is it indicated?

Does it improve mortality in this context?

A

Epleronone is aldosterone antagonist (like spironolactone) and indicated in:

post-MI + LV-dysfunction + HF

Improves mortality.

68
Q

What is Ivabradine and when is it indicated?

What conditions are required for it’s use?

A

Inhibition of ‘funny’ channel in the SAN and used to treat chronic stable angina with intolerance or contraindication to beta-blockers:

Requires the following:
SR
LVEF less than 35%
HR greater than 70

69
Q

What are the 4 criteria for Biventricular-pacing?

A

Criteria for Bi-V PPM:

  1. Wide QRS > 120ms
  2. LVEF
70
Q

What are the 4 targets of treatment with biventricular pacing?

A
  1. 100% pacing
  2. Atrial tracking
  3. LV-filling optimisation
  4. Decrease ventricular arrhythmias
71
Q

Describe AICD for primary and secondary prevention.

What is the life-expectancy parameter prior to AICD insertion?

A

Primary prevention:

  1. NYHA > 2
  2. LVEF 40d post-MI

Secondary prevention:
Demonstrated ventricular arrhythmias

MUST have life expectancy > 1 year.

72
Q

Which 5 clinical features suggests poor prognosis in a patient with cardiomyopathy?

A
  1. NYHA IV
  2. Syncope
  3. Persistent S3
  4. RHF
  5. Symptomatic VT
73
Q

Which 4 biochemical features confer suggests poor prognosis in a patient with cardiomyopathy?

A
  1. Hyponatraemia
  2. Elevated BNP
  3. Elevated noradrenaline
  4. MVO2
74
Q

What are 3 cath-lab or echo findings that suggest poor prognosis in a patient with cardiomyopathy?

A
  1. PCWP > 20 mmHg

2. Low CI

75
Q

How is cardiac index (CI) calculated?

A

CI = CO x BSA

CO = cardiac output
BSA = body surface area

CO = SV x HR

76
Q

At what age is heart transplantation no long considered an option?

A

Usually

77
Q

Under which 4 circumstances is a heart transplant indicated?

A
  1. VO2 max
78
Q

Patient has LVEF

A

No.

79
Q

Patient has a history of ventricular arrhythmias.

May he upon this information have a heart transplant?

A

No.

80
Q

Patient has VO2max > 15 ml/kg/min.

May he upon this information have a heart transplant?

A

No.

81
Q

Patient has VO2max = 13 ml/kg/min and cannot tolerate beta-blockers.

May he upon this information have a heart transplant?

A

Sure - go for it.

82
Q

List 4 categories of contradindications for heart transplantation.

A
  1. Active disease (5): cancer, infection, substance abuse, Hep B/C, HIV.
  2. Organ damage (5): DM-related, kidney, liver, lung, CNS (degenerative)
  3. Compliance
  4. Habitus: BMI > 30
83
Q

What is the MOST likely causes of DEATH post heart transplantation at:

a.

A

a.

84
Q

What are the 4 long term complications post heart transplantation?

A

Dr Mac (DRMC):

DM
Renal
Malignancy
Coronary vasculopathy

85
Q

Which of the long-term complications post heart transplantation is more likely at:

a. 1 yr
b. 5 yrs
c. 10 yrs

A

RDC:

a. 1 yr: Renal = DM > CV > M
b. 5 yrs: DM > Renal = CV > M
c. 10 yrs: CV > Renal = DM > M

DRMC: DM, renal, malignancy, coronary vasculopathy

86
Q

What are the survival rate post heart transplantation at:

a. 1 yr
b. 5 yrs
c. 10 yrs

A

a. 1 yr > 80%
b. 5 yrs > 70%
c. 10 yrs = 60%

87
Q

Which pathogen is implicated in coronary allograft vasculopathy post heart transplantation?

Comment on the pathophysiology.

A

CMV

endothelial injury causes intimal hyperplasia and vascular smooth muscle proliferation.

88
Q

What is the palliative pharmacotherapy heart transplant patients complicated by coronary vasculopathy?

A

MCS:

mTOR inhibition (Sirolimus / Everolimus)
CCB (Diltiazem)
Statin

89
Q

True/False: Tacrolimus has the same MOA as Sirolimus.

A

False - different MOA (sound similar)

Tacrolimus = macrolide calcineurin inhibitor causing IL-2 inhibition.

Sirolimus (like Everolimus) = mTOR inhibitors causing IL-2 inhibition.

90
Q

In the prevention of rejection in heart transplantation which chemotherapy agents blocks the following parts of the T-cell cell cycle and regulation:

G0 resting
G0 to G1
G1 to S
S to M

IL2 receptor

A

G0 resting:
Anti-thymocyte globulin (ATG) - causes depletion of T-cells
OKT3 - inhibition of TCR recognition

G0 to G1: Cyclosporin A, Tacrolimus - calcineurin inhibition.

G1 to S: Sirolimus, Everolimus - mTOR inhibition leading to IL-2 inhibition

S to M: Azathiprine, Mycophenolate (MMF) - inhibition of nucleotide synthesis

IL2-receptor: Silmulect, Basiliximab

91
Q

What is the likelihood of acute rejection post heart transplantation?

A

20-50%

92
Q

Which regimen of immunosuppression post heart transplantation confers the lowest rejection rates?

A

Tacrolimus and cyclosporin containing regimens.

93
Q

What is first-line and second-line immunosuppression therapy in heart transplantation?

A

1st line (CMP): cyclosporin/tacrolimus + MMF + prednisone

2nd line: Sirolimus / Everolimus

94
Q

What drug interactions should be considered with usage of calcineurin inhibitors or mTOR inhibitors?

A

Drugs that affect CYP3A4:

Inducers lead to decreased drug levels.

Inhibitors lead to increased drug levels.

95
Q

What are the 6 ABSOLUTE contraindications for thrombolysis in a STEMI patient?

A

In last 3 months (2):

  1. CVA
  2. Head or facial trauma

At anytime:

Brain (3):

  1. ICH
  2. AV-malformation
  3. Brain malignancy

Non-brain:
6. Suspected aortic dissection

96
Q

Which leads are involved in a STEMI of the PDA (posterior descending artery)?

A

PDA = ST depression in V1 - V4 (anterior leads) with a dominant R-wave in V1 (supplies the LV)

97
Q

Which leads are involved in a STEMI of the RCA?

A

RCA = II, III and aVF (inferior leads)

98
Q

Which leads are involved in a STEMI of the left main origin?

A

LCx = I, aVL, V5, V6

plus

LAD = V1 - V4

Therefore: ST elevation in all praecordial leads (V1 - V6), I and aVL.

99
Q

Which leads are involved in a STEMI of the LAD?

A

LCx = V1 - V4 (antero-septal) with reciprocal ST depression in inferior leads, due to watershed ischaemia to territories supplied by LAD.

100
Q

What are the risk factors for bleeding when considering antiplatelet therapy and antithrombotic medications (4)?

A
  1. Old age
  2. Renal impairment
  3. Known bleeding disorder
  4. Underweight

All except 4 pretty obvious.

101
Q

True/False: If used with the right indication, Ivabradine has mortality benefit.

A

True.

102
Q

What are the ECG findings of Brugada syndrome?

What test is used to elicit Brugada?

A

Type 1 - coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave (Brugada sign - most useful)

Type 2 - has >2mm of saddleback shaped ST elevation.

Type 3 - can be the morphology of either type 1 or type 2, but with

103
Q

What conditions are associated with the following 6 channelopathies?

Beta MHC (myosin heavy chain)
LMNA
SCN5A loss of function Na channels
SCN5A gain of function Na channels
KCNQ1
KCNQ2
A

Beta MHC (myosin heavy chain) = HOCM

LMNA = DCM (lamin A or C genes)

SCN5A ‘loss’ of function Na channels = Brugada

SCN5A ‘gain’ of function Na channels = LQT3

KCNQ1 = LQT1
KCNQ2 = LQT2
104
Q

What are the 5 signs of severe aortic stenosis?

Which of these is most important?

A

‘I am APaLLD that you don’t know the signs of severe AS!’

A2 absent
Pressure-load apex beat
Late-peaking murmur (most important)
Length of murmur
Delayed carotid upstroke
105
Q

What is the MOA of flecainide?

A

Block Na channels

NB:

  • Brugada = channelopathy with loss of function in Na channels (SCN5A)
  • Giving Flecainide exacerbates this abnormality.

Class 1C antiarrhythmic

106
Q

True/False: In a patient with Heyde’s Sydrome, AVR will reduce bleeding risk in the patient.

A

True.

Heyde’s Syndrome: AS causing type IIa vWD and GI bleeds from angiodysplasia. Bleeding improves after AVR.

107
Q

What is the medical treatment of a symptomatic HOCM with LVOT obstruction and signs of HF?

Which agent is most preferred?

What agents need to be avoided?

A

Monotherapy with negative ionotrope:

Beta-blocker (best option)
Non-dihydropyridine calcium channel blocker (e.g. verapamil)
Disopyramide

Avoid vasodilators and diurectics

108
Q

What is the medical treatment of a asymptomatic HOCM with LVOT obstruction?

A

Nothing - just monitor.

109
Q

What are 3 echo findings of HOCM?

A

LOVE MR SAM ASH:

LVOT obstruction

Mitral Regurgitation

Systolic Anterior Motion of the anterior mitral leaflet

Asymmetric Septal Hypertrophy

110
Q

What is the inheritance pattern of HOCM?

What is the significance of this?

A

Autosomal dominant with high penetrance.

Therefore 1st degree relatives of affect individual need to be screened.

111
Q

What is a SE of Ivabradine?

A

Bright spots in the vision that comes and goes.

112
Q

What is the treatment of infective endocarditis in the following scenarios:

  1. Native valve (normal vs. hospital-acquired/IVDU)
  2. Prosthetic valve
A
  1. a. normal: gentamicin + benzylpen + fluclox
    b. abnormal: gentamicin + vanc + fluclox
  2. gent + vanc + fluclox
113
Q

How are the types of LQTS best remembered in terms of types of channels involved and clinical context.

A

LQTS 1 = slow K channels, swimming/exercise
LQTS 2 = fast K channels, stress-induced
LQTS 3 = Na channels, sleeping

Mnemonic phrase:
A Slow swim puts you to death
A Fast life puts you to death
Sod it, even sleep puts you to death

NB:
puts = potassium
sod = sodium

114
Q

Patient presents with WPW and AF:

  1. What drugs should be avoided? Why?
  2. Which drugs are used in treatment of stable WPW?
  3. What is the treatment of unstable WPW?
  4. What is the definitive treatment of WPW?
A 
1. Drugs that block the AVN - ABCD(L)
Adenosine
Beta-blockers
Calcium channel blockers
Digoxin 
Lignocaine
NB: drugs that are normally considered in the treatment of AF/SVT
  1. Amiodarone and Flecainide (Mnemonic = AF)
  2. DC cardioversion
  3. EPS and ablation
115
Q

What is the treatment of LQST?

A

Beta blockers.

FRACP (20 decks)

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