The Basics Flashcards

1
Q

What are the three primary causes of AS (from most to least common)?

A
  1. Calcific (most common)
  2. Rheumatic
  3. Congenital (least common)
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2
Q

What are the types of bicuspid aortic valve?

A

Type 0: 0 raphe, true BAV
Type 1: 1 raphe (most commonly raphe between RCC and LCC)
Type 2: 2 raphe (functionally unicuspid)

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3
Q

What is a raphe?

A

Seam/fibrous ridge between two cusps (also known as a false commissure)

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4
Q

Which is the most common type of BAV?

A

Type 1 (one raphe) with raphe between the right and left coronary cusps

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5
Q

Prevalence of AS in patients < 50 years old?

A

AS patients < 50 years old are likely to have a bicuspid AV

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6
Q

Prevalence of AS in patients > 70 years old?

A

AS patients > 70 years old are likely to have a tricuspid AV

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7
Q

Progression: How does AV sclerosis become calcific AS?

A

Three stages:

  1. Endothelial Damage
  2. Fibrosis
  3. Calcification
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8
Q

Initiating factors of AS

A
  1. Mechanical stress
  2. Bicuspid aortic valve
  3. Genetic factors
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9
Q

Risk factors for AS

A
  1. Older age
  2. Male
  3. Hypertension
  4. Diabetes
  5. Smoking
  6. Metabolic syndrome
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10
Q

Haemodynamic Consequences of AS

A
  1. Adaptation of the left ventricle
  2. Left atrium
  3. Cardiac output
  4. Perfusion
  5. End-stage
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11
Q

Haemodynamic Consequences of AS: Adaptation of the Left Ventricle

A
  1. Increased LV systolic pressure leading to concentric hypertrophy
  2. Decreased LV compliance
  3. Increased filling pressures
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12
Q

Haemodynamic Consequences of AS: Left Atrium

A
  1. LA dilatation (as a result of decreased LV compliance and increased LV filling pressures)
  2. Increase in LAP
  3. Can lead to development of AF
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13
Q

Haemodynamic Consequences of AS: Cardiac Output

A
  1. Initially normal CO (due to compensatory mechanisms)

2. CO declines as disease progresses

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14
Q

Haemodynamic Consequences of AS: Perfusion

A

Decreased CO leads to decrease in 1) myocardial and 2) cerebral perfusion

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15
Q

Haemodynamic Consequences of AS: End-Stage

A
  1. Reduction in LV contractile function
  2. Pulmonary hypertension
  3. RV dysfunction
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16
Q

What are the ‘classic’ symptoms of AS?

A
  1. Angina
  2. Syncope
  3. Heart failure
17
Q

What causes angina?

A

Due to decreased myocardial perfusion and ischemia

18
Q

What causes syncope?

A

Due to decreased cerebral perfusion

19
Q

What causes heart failure?

A

Due to the inability of the heart to supply sufficient blood flow to meet the needs of the body

20
Q

What are the early but non-specific symptoms of AS?

A
  1. Exertional dyspnoea (decreased exercise tolerance)
  2. Exertional dizziness (pre-syncope or syncope)
  3. Exertional angina
21
Q

What are the management strategies for AS?

A

Management strategies consider stages, diagnosis, medical therapy and interventions

22
Q

What categories are the stages of AS defined by?

A

Each stage is defined by:

  1. Valve anatomy
  2. Valve haemodynamics
  3. Haemodynamic consequences
  4. Symptoms
23
Q

What are the interventional options for patients with severe AS?

A

SAVR - surgical AV replacement

TAVR - trans catheter (trans femoral) AV replacement

24
Q

What are other causes of LV Outflow Obstruction?

A

Subvalvular AS and supravalvular AS

25
Q

What is subvalvular AS?

A

Obstruction below AV (in LVOT)
Can be fixed or dynamic obstruction
Fixed obstruction: discrete fibrous membrane, fibromuscular ridge, fibromuscular tunnel (with septal hypertrophy and thickened amvl)
Dynamic obstruction: HOCM with ASH and SAM

26
Q

What is supravalvular AS?

A

Obstruction above AV (distal - on aortic side)
Morphological types: hourglass deformity (most common), fibrous membrane, diffuse hypoplasia ascending aorta
Most often seen in William syndrome