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1
Q

Which measurement is most critical for TAVI valve sizing?

A

Aortic annulus diameter measured from inner edge to inner edge at the base of cusps

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2
Q

What is the key diagnostic criterion for isolated ventricular non-compaction?

A

Ratio of non-compacted:compacted myocardium >2

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3
Q

What are the major criterion for ARVC?

A

Major Echocardiographic Criteria

Regional RV akinesia, dyskinesia or aneurysm
AND one of the following:

•	RV outflow tract (RVOT) dilatation
•	Parasternal long-axis view: RVOT >32 mm (PLAX) or indexed >19 mm/m²
•	Parasternal short-axis view: RVOT >36 mm (PSAX) or indexed >21 mm/m²

OR
• RV fractional area change (FAC) <33%

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4
Q

What are the minor criteria for ARVC?

A

🟨 Minor Echocardiographic Criteria

Regional RV akinesia or dyskinesia
AND one of the following:

•	Mild RVOT dilatation
•	PLAX: 29–32 mm or indexed 16–19 mm/m²
•	PSAX: 32–36 mm or indexed 18–21 mm/m²

OR
• RV FAC 33–40%

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5
Q

What is the WALLS mnemonic in LV true vs pseudoaneurysm?

A

To recall differences between true and pseudoaneurysm:
• Wall continuity:
• True = myocardium
• False = pericardium only
• Aneurysm neck:
• True = Wide
• False = Narrow
• Location:
• True = Anterior/apical
• False = Posterior/inferior
• LV motion:
• True = Dyskinetic
• False = Paradoxical (sac-like)
• Surgery:
• True = Often elective
• False = Urgent

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6
Q

Normal rate of PFO?

A

15% positive bubble study in normal population
- bubbles in LA within 3 cycles of the contrast in the RA

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7
Q

SVC vs ASD flow

A

ASD flow peaks in late diastole and systole

SVC peaks are earlier

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8
Q

Causes of bi atrial enlargement

A

Chronic AF
Restrictive cardiomyopathy
Rheumatic heart disease of MV & TV
Athletic heart (only mild enlargement)
Pericardial constriction

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9
Q

Predominant LA enlargement

A

MR or MS
LV diastolic dysfunction (LVH/AS/AR)

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10
Q

Causes of RA dilation

A

TS / TR
PHTN
ASD
RV cardiomyopathy

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11
Q

What are the echo findings of familial dilated cardiomyopathies?

A

Duchennes/Beckers MD
- inferolateral akinesia
- AV block
- ventricular arrhythmias

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12
Q

Causes of dilated hyperkinetic LV

A

Valve disease
- severe AR / MR
- moderate or worse mixed AR + MR

Shunts
- VSD
- ruptured sinus of valsalva aneurysm
- persistent ductus

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13
Q

Echo features of athletic heart

A

Can persist >5 years after stopping training

  • Increased LVDd (rarely >60mm)
  • normal systolic function, possible borderline global hypokinesis
  • normal LV diastolic function
  • mild RV dilation and hypertrophy
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14
Q

Echo findings in sarcoidosis

A
  • dilated LV with global systolic dysfunction
  • RWMA not in a coronary artery distribution
  • thin walls (commonly basal anterior septum)
  • LV aneurysms
  • diastolic dysfunction
  • focal intracardiac mass (granuloma)
  • RV dysfunction secondary to pulmonary disease
  • pericardial effusion
  • high incidence of arrhythmias
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15
Q

Causes of acquired DCM

A

Tachyarrhythmia
Alcohol
Drugs
Autoimmune (SLE, Churg-Strauss)
Sarcoid
Peripartum cardiomyopathy
Haemachromatosis
Thalassaemia
HIV
Thiamine deficiency
Hypothyroidism
Post myocarditis (viral/kawasaki)

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16
Q

Echo findings in autoimmune DCM

A

Impaired LV relaxation
MR
Pericardial effusion
Valve thickening
Non bacterial Libman-Sacks vegetations
Pulmonary hypertension
Pericardial effusion

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17
Q

Differentiating primary and secondary MR with a dilated LV

A
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18
Q

Common causes of LV hypertrophy

A

Hypertension
Aortic stenosis
Renal disease
Afro Caribbean ethnicity
Obesity
Athletes (usually only mild)

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19
Q

Cardiomyopathies causing LVH

A

Hypertrophic cardiomyopathies
Metabolic genetic errors
- glycogen storage (pompe, Danon)
- lysosomal storage (Anderson-Fabry)
- carnitine disorders
- AMP-kinase (PRKAG2)
Infiltrative disorders (amyloidosis)
Neuromuscular (e.g friedrich’s ataxia)
Malformation (Noonan’s)
Mitochondrial disease
Drug induced (tacrolimus, hydroxychloroquine, steroids)

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20
Q

HCM echo features

A

Asymmetrical hypertrophy

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21
Q

Where does ARVC normally affect?

A

Infundibulum
Apex
Wall
Peri TV area

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22
Q

Distinguishing feature for restrictive cardiomyopathy from constrictive pericarditis

A

Presence of septal bounce during respiration

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23
Q

Most reliable measure for AS severity when other measures are discordant

Study These Flashcards
A

Effective orifice area using continuity equation

24
Q

Echo signs of amyloid

Study These Flashcards
A

Concentric LVH with ground glass myocardial appearance

25
Causes of non HOCM SAM
26
Causes of non HOCM SAM
27
Features of HOCM rather than hypertensive heart
28
29
Features of cardiomyopathy rather than athletes heart
- Asymmetric hypertrophy mainly affecting septum - wall thickness >15mm - no change in 3-5 months post detraining - involvement of Rv and LV
30
Non HOCM phenocopies and their features
31
Definition of restrictive cardiomyopathy
No LVH No LV Dilation Restrictive filling - E/A >2.5, DTE <140, E/e' >14 Normal or mildly reduced LV function
32
What are the causes of restrictive cardiomyopathy?
33
Non-compaction - description and diagnosis
Normal myocardium compacts / loses trabeculation Non-compaction can be associated with other congenital heart defects
34
Echo signs of ARVC
35
Chemo and echo monitoring
36
What is the Doppler frequency shift equation?
Delta f = (2 f_0 v x cos theta) b (c) Where: • \Delta f = Doppler frequency shift (Hz) • f_0 = Transmitted frequency of the ultrasound (Hz) • v = Velocity of blood flow (m/s) • \theta = Angle between the ultrasound beam and the direction of blood flow • c = Speed of sound in tissue (~1540 m/s) ⸻ Rearranged to Solve for Velocity: v = (Delta f x c) / (2 x f_0 cos theta)
37
Attenuation rule of thumb
Attenuation Rule of Thumb: Attenuation} ~ 0.5 dB/cm/MHz
38
What are the nodules of Arantius?
nodules of Arantius are small fibrous structures located at the center of the free edge of each aortic valve cusp. They are key anatomical features of the aortic valve and help ensure proper valve closure. ⸻ 🔹 Anatomical Summary: • Each of the three aortic valve cusps (right, left, and non-coronary) has: • A lunule (a thin, fibrous margin) • A central thickening called the nodule of Arantius ⸻ 🔹 Function: • The nodules of Arantius meet centrally when the valve closes during diastole. • This enhances coaptation, forming a tight seal to prevent aortic regurgitation. • Without these nodules, small central leaks could occur due to imperfect leaflet closure. ⸻ 🔹 Clinical Relevance: • Important in: • Valve anatomy for surgical and transcatheter aortic valve implantation (TAVI/TAVR) • Understanding central vs. eccentric aortic regurgitation jets • Rare cases of Lambl’s excrescences (filamentous strands on nodules) ⸻ 🧠 Mnemonic Tip: Think: “A for Arantius, A for Aortic valve”
39
Doppler shift equation
Doppler shift = transducer frequency x 2 x cos (angle of beam/flow) / speed of sound
40
Mean pressure gradient equation
2.4 x Vmax^2
41
Systemic vascular resistance calculation
SVR = (MAP - RAP) / CO ALSO SVR = (1.33 x mean pressure gradient x systolic ejection time ) / stroke volume
42
Cardiac complications of Kawasaki disease
Coronary artery aneurysms
43
Cardiac complications of takayasu’s
Aortic aneurysms
44
What are carcinoid tumours and why do they only affect the right side of the heart?
Metastatic carcinoid tumour to the liver secretes 5HT / Serotonin products that affect right heart valves but are degraded in the lungs and therefore do not affect the left heart unless there is a right to left shunt
45
What are the cardiac complications of alagille syndrome
Cardiac Involvement • Most commonly peripheral pulmonary artery stenosis • Can also involve: • Tetralogy of Fallot • Pulmonary atresia • Other complex congenital heart disease
46
Why does VSD not cause RV dilation?
Left to right shunt goes directly into the PA so does not cause volume overload. VSD alone with dilated RV suggests need to look for alternative cause E.g. ASD
47
How do you calculate PAP in pulmonary stenosis?
PAP = [[4VTR^2 + RAP] - 4(VPS)^2 You need to compensate for the additional backflow gradient of the pulmonary stenosis.
48
What are the TTE features of amyloid?
Concentric LVH Ground glass appearance of the myocardium Thickened valves and IAS Thickened RV wall Marked reduced GLS with apical sparing Low ECG voltage Pericardial effusion
49
TTE features of Fabry disease
LV hypertrophy (can be asymmetrical) Global hypokinesia +/- dilated LV Inferolateral mid-wall scarring Thickened valves Thickened RV wall
50
How to define restrictive cardiomyopathy
Restrictive filling - mitral deceleration time <140ms - mitral E/A >2.5 - average E/E' > 14 Normal or mildly reduced LV systolic function No obvious LVH or dilation
51
Causes of restrictive cardiomyopathy
Amyloid Sarcoid Fabry Pompe Mucopolysaccharidosis Haeamachromatosis Endomyocardial fibrosis Cancer and cancer therapies
52
Features of endomyocardial fibrosis
Echogenicity at RV or LV apex Sub-valve LV or RV thickening LV / RV thrombus TR / MR
53
Why is the diagnostic test for amyloidosis?
99mTc-DPD scintigraphy
54
TTE findings of LV non compaction
- > 3 prominent trabeculations - Ratio non- compacted: compacted > 2 on end systolic Parasternal short axis Associated with: - heart failure - ventricular arrhythmia - systemic emboli Often a family history
55
56
TTE changes in ARVC
RV dilation Reduced RV systolic function RWMA (akinesis, dyskinesia or aneurysm) Most commonly - infundibulum, apex, inferolateral wall and peri tricuspid annulus

EACVI (4 decks)

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