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chest FRCR > Cardiac > Flashcards

Cardiac Flashcards

1
Q

Why would lipomatous hypertrophy of IA septum be hot on PET?

A

Because it has brown fat.

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2
Q

Branches of LCA:

A

LAD: Diagonal and septal branches LCx: Obtuse marginal- supply lateral margin.

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3
Q

Branches of RCA:

A

Acute marginal AV node (90%) and SA node (60%) PDA- 65-80%

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4
Q

What determines the dominance on coronary arteries?

A

What supplies the PDA and posterior LV branches determines the dominance.

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5
Q

What is the treatment in the following disarrangement? 1) RCA arising from the left coronary sinus? 2) LCA arising from the right coronary sinus?

A

1) RCA arising from the left coronary sinus: REPAIR if symp. 2) LCA arising from the right coronary sinus: ALWAYS REPAIR

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6
Q

ALCAPA stands for?

A

Anomalous LCA from the pulmonary artery.

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7
Q

What is a STEAL SYNDROME?

A

It is reversal of flow in the LCA as pressure decreases in pulmonary circulation.

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8
Q

Causes of coronary artery aneurysm?

A
  1. Atherosclerosis 2. Kawasaki- resolves in 50% 3. Iatrogenic by cardiac catheters.
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9
Q

Who is the ideal patient to get a coronary CT? (2)

A

1) Low risk or atypical chest pain 2) Suspected aberrant coronary anatomy.

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10
Q

What is the ideal heart rate?

A

Low heart rate is optimal to reduce artefact. BB are used to achieve HR<60.

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11
Q

to BB? (4)

A

Severe asthma Heart block Acute chest pain Cocaine

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12
Q

Are all heart blocks # to BB?

A

NO! 2nd and 3rd are # A 1st degree block is ok. If cant give BB: can only do retrospective gating

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13
Q

What is the difference between retrograde and prospective gating?

A

Prospective: Step and Shoot, use RR interval as tigger +ve: Low radiation dose -ve: No functional images Trivia: Always axial and not helical Retrospective: scan the whole time and the recalculate +ve: Functional images -ve: High radiation dose, use low pitch= high dose Trivia: Helica.

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14
Q

Any other drugs than BB given for coronary CT?

A

GTN to dilate the coronaries.

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15
Q

to GTN? (4)

A

Hypotension: SBP<100 Severe aortic stenosis HOCM Phosphodiesterase (viagra Sildenafil) use

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16
Q

Name the sequence used for quantifying the velocity of flowing blood;

A

Velocity encoded cine MR imaging (VENC) also known as velocity mapping or phase contrast imaging.

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17
Q

Name the causes of ascending aortic dilatation: (3)

A
  1. Supravalvular: Williams syndrome 2. Valvular 90% 3. Subvalvular
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18
Q

Supravalvular aortic stenosis…

A

William’s syndrome

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19
Q

Bicuspid aortic valve and coarctation…

A

Turner’s syndrome

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20
Q

Most common congenital heart disease:

A

Bicuspid aortic valve and VSD

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21
Q

What are the associations with bicuspid aortic valve: (3)

A

Polycystic kidney disease CMN: cystic medial necrosis Turner’s syndrome and coarctation. Increases the risk of aortic aneurysm.

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22
Q

Causes of aortic regurgitation: (5)

A
  1. Bicuspid aortic valve 2. Bacterial endocarditis 3. Marfans 4. Aortic root dilation secondary to HTN 5. Aortic dissection
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23
Q

Most common cause of mitral regurgitation:

A

Rheumatic heart disease

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24
Q

What are the signs of MR on CXR:

A

LA enlargement: - Double density sign - Splaying of the carina - Posterior oesophageal displacement

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25
Q

What causes mitral regurgitation?

A

Acute: - Endocarditis - Papillary muscle/chordae rupture post MI Chronic: - Primary: Myxomatous degeneration - Secondary: Dilated cardiomyopathy

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26
Q

Isolated RUL pulmonary oedema is associated with…

A

Mitral regurgitation.

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27
Q

Pulmonary stenosis syndrome:

A
  1. uSpravalvular: Williams syndrome 2. Valvular: Noonan’s syndrome (male version of Turner’s) 3. Subvalvular- TOF
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28
Q

Peripheral pulmonary stenosis is seen with…

A

Alagille syndrome: Absent bile ducts

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29
Q

Most common cause of PR

A

TOF patients with repair.

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30
Q

Which valves most commonly affected by rheumatic heart disease?

A

MV and AV Multivalve disease, think of rheumatic fever.

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31
Q

Rh heart disease is immune modulated response to which group of infection?

A

Group A beta haemolytic strep.

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32
Q

Causes of Tricuspid regurgitation:

A
  1. Endocarditis (IVDU) 2. P HTN 3. Carcinoid ( Serotonin degrades the valve)
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33
Q

What happens to RV in TR?

A

RV dilation and NOT hypertrophy.

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34
Q

Which children are at increased risk of Ebstein anomaly?

A

Children whose mums used Lithium

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35
Q

What happens in Ebstein anomaly?

A

The TV is hypoplastic , the posterior leaf is displaced apically (downwards) –> Enlarged RA, decreased RV(atrialised) and TR.

Massive box shaped heart on CXR

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36
Q

When would tricuspid atresia happens?

A

It happens with RV hypoplasia

There is almost always an intra-atrial connection through:

  • ASD or
  • PFO
  • A small VSD is often also present.
  • +/- transposition of great arteries (TGA).
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37
Q

Associated findings with TA (tricuspid atresia)

A
  1. ASD and
  2. PFO -
  3. Right sided arch (think of truncus and TOF) -
  4. Asplenia
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38
Q

TA and PS?

A

TA + PS = reduced vascularity

TA alone = increased vascularity

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39
Q

Which side of the heart gets affected by carcinoid syndrome?

A

Right side of the heart: Tricuspid and pulmonary

Left side is super rare.

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40
Q

How would carcinoid syndrome affects the valves?

A

The serotonin degrades the valve- usu the right side

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41
Q

What does it mean if you see a left sided valvular disease with carcinoid syndrome? (2)

A
  1. Primary bronchial carcinoid
  2. Right to left shunt
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42
Q

The terminology right arch/left arch is based on relationship of aortic arch to which structure?

A

Trachea

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43
Q

When I say right arch with mirror branching, you say…

A

Congenital heart

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44
Q

What is a Bovine arch?

A

This is when the BCA and LCCA arise from a common origin.

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45
Q

If there is mirror image right arch, then 90% will have…

A

TOF 6% truncus

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46
Q

If a person has truncus , then they have a mirror image right arch…

A

33% TOF 25%

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47
Q

What symptoms patients with aberrant RSCA most likely to present with?

A

Dysphagia lusoria

As the RSCA passes posterior to oesophagus

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48
Q

What is a Kommerell diverticulum?

A

It refers to the bulbous configuration of the origin of an aberrant left subclavian artery in the setting of a right sided aortic arch.

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49
Q

What are the symptoms of double arch? Location?

A

Tracheal compression and dysphagia. Arches are posterior to esophagus and anterior to trachea- encircling them both.

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50
Q

Subclavian Steel Phenomenon?

A

Stenosis and/or occlusion of the proximal subclavian with retrograde flow in the ipsilateral vertebral artery.

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51
Q

Subclavian Steel Syndrome?

A

Stenosis and/or occlusion of the proximal subclavian artery with retrograde flow in the ipsilateral vertebral artery AND associated cerebral ischaemic symptoms (syncope, dizziness etc).

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52
Q

What are the causes of SSS? (5)

A
  1. Atherosclerosis
  2. Takayasu arteritis
  3. Radiation
  4. Preductal aortic coarctation
  5. Blalock Taussig shunt
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53
Q

What are the causes of cyanosis in paediatric patients? (5)

A
  1. Truncus
  2. TOF
  3. Transposition
  4. Tricuspid atresia
  5. TAPVR
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54
Q

Come up with the diagnosis:

Cyanosis, Right sided arch with increased blood flow.

A

Truncus

ie Single trunk supplies both the pulmonary and systemic circulation, instead of a separate aorta and a pulmonary trunk

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55
Q

Come up with the diagnosis:

Cyanosis, right sided arch with reduced blood flow.

A

TOF

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56
Q

Come up with the diagnosis:

Cyanosis, left sided arch with massive heart size

A

Ebstein

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57
Q

Come up with the diagnosis:

Cyanosis, left sided arch with increased blood flow

A
  1. TAPVR
  2. Transposition
  3. Tingle ventricle.
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58
Q

Come up with the diagnosis:

Cyanosis, left sided arch with decreased blood flow

A
  1. Ebstein
  2. Tricuspid atresia
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59
Q

What are the causes of non-cyanotic peadiatric patient with CHD (5)

A
  1. ASD
  2. VSD
  3. PDS
  4. PAPVR
  5. Aortic coarctation- adult type
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60
Q

What are the DDx for small heart? (3)

A
  1. Adrenal insufficiency - Addison’s
  2. Cachectic state
  3. Constrictive pericarditis
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61
Q

Re VSD: -

Most common types

  • Which type must be repaired?
  • CXR findings?
A
  • Most common congenital heart disease - Membranous type most common.
  • The outlet subtypes (infundibulum) must be repaired as the right coronary cusp prolapses into the defect. -
  • Non specific:
  • Cardiomegaly,
  • increased vasculature,
  • small aortic knob or
  • LA enlargement.
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62
Q

When does PDA close?

A

Usually closes after 24 hours after birth (functionally) and anatomically around 1 month.

Can close it or keep it open with medication.

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63
Q

PDA is associated with… ? (3)

A
  1. Prematurity
  2. Maternal rubella
  3. Acyanotic heart disease
64
Q

When I say hand/thumb defect + ASD, you say…

A

Holt Oram

65
Q

When I say ostium primum ASD, you say…

A

Down’s syndrome

66
Q

When I say sinus venosus ASD, you say…

A

PAPVR

67
Q

What does AV canal refer to?

A

Endocardial cushion defect

68
Q

What causes the development of the AV canal?

A

Secondary to deficient development of a portion of atrial septum, a portion of IV septum and AV valve.

69
Q

What is the strong association of AV canal?

A

Down’s syndrome

70
Q

What is an unroofed coronary sinus?

Most common clinical findings?

A

Rare ASD which occurs secondary to a fenestrated or totally unroofed coronary sinus.

Paradoxical emboli and chronic right heart volume overload.

71
Q

What is the strong association of unroofed coronary sinus?

A

Persistent left sided SVC.

72
Q

What is a TAPVR? What is needed for survival?

A

This is when the pulmonary venous system drains to the right side of the heart.

PFO or ASD is required.

73
Q

What are the different types of TAPVR? (3)

A
  1. Type 1: Supracardiac: Most common type Veins drain above the heart = snow man appearance
  2. Type 2: Cardiac: Second most common type
  3. Type 3: Infracardiac: Veins drain below the diaphragm: Hepatic veins or IVC. Obstruction on the way back is common and causes a full on pulmonary oedema look.
74
Q

What are the congenital heart disease associated with asplenia?

A

50% would have CHD:

  • 100% would have TAPVR and
  • 85% have additional endocardial cushion defect.
75
Q

What is PAPVR?

What is it associated with?

A

Partial Anomalous Pulmonary Venous Return. This is when one or more of the 4 Pulmonary veins drain into the right atrium.

It is associated with ASD.

76
Q

When I say right sided PAPVR, you say..

A

Sinus venous ASD

RUL: SVC association with sinus venous type ASD

77
Q

When I say Right sided PAPVR and pulmonary hypoplasia , you say..

A

Scimitar syndrome

78
Q

What is the main RF for transposition

A

Maternal diabetes

79
Q

How can you tell which chamber is the RV?

A

The one with the moderator band is the right ventricle.

80
Q

What are the different types of transposition? Which one needs correction?

A
  1. D type- You need patent PDA. Intra-atrial baffle (Mustard or Senning procedure) is performed to fix them
  2. L type- L type is Lucky enough to be congenitally corrected. There is inversion of the ventricles - No PDA is needed.
81
Q

What happens in L type transposition?

A

Aorta –> Systemic–> RA–> LV–> PA–> Lungs–> LA–> RV–> Aorta

82
Q

What happens in D type transposition?

A

Aorta–> systemic–> RA–> RV–> Aorta { PDA { PA–> lungs–> LA–> LV–> PA

83
Q

What is a corrected D transposition?

A

This is when the PA is draped over the aorta which occurs after a surgeon has performed “ LeCompte Maneuver”

84
Q

What is the tetralogy of Fallot?

A
  1. VSD
  2. RVOTO (Right Ventricular Outflow Tract Obstruction)
  3. Overriding aorta
  4. RV hypertrophy
  5. If there is ASD- Pentalogy of Fallot- likely to have Right arch
85
Q

What is the most common complication post TOF repair?

A

Pulmonary regurgitation.

86
Q

What is a truncus arteriosus?

A

This is when single trunk supplies the systemic and pulmonary circulation.

Almost always has a VSD.

Associated with Right arch.

87
Q

What is truncus associated with?

A

CATCH 22 genetics (Di George syndrome)

88
Q

Define coarctation?

What are the types?

CXR sign?

A

This is narrowing of the aortic lumen.

Two flavours:

  1. Infantile (preductal)- pulmonary oedema
  2. Adult (ductal) Figure 3 sign and rib nortching (4th - 8th ribs) on CXR.

It does not involve the 1/2 rib because they are fed by costocervical trunk.

89
Q

What are the associations with coarctation?

A
  1. Turner’s syndrome
  2. Bicuspid aortic valve- 80%
  3. Berry aneurysm
90
Q

Re Hypoplastic left heart:

What is it?

A

This is when the LV and aorta are hypoplastic. They present with pulmonary oedema. Must have ASD/PFO or a large PDA

91
Q

What is hypoplastic left heart associated with? (2)

A
  1. Aortic coarctation
  2. Endocardial fibroelastosis.
92
Q

Cor Triatriatum Sinistrum

A

This is when an abnormal pulmonary vein drains into the LA (sinistrum means left) with unnecessary fibromuscular membrane that causes a subdivision of the LA creating the appearance of a tri-atrium heart.

93
Q

What is the main signs and symptoms of Triatriatum Sinistrum

A
  1. Unexplained pulmonary hypertenion in paeds
  2. Acts like MS - Pulmonary oedema

Prognosis is bad, fatal within 2 years.

94
Q

Where does the wave front of necrosis start?

A

The wave front of necrosis always starts sunendocardial and progresses to subepicardium.

Delayed enhancement follows a vascular distribution.

95
Q

How would acute/subacute MI look like on MR?

A

Micovascular obstruction: destruction of small capillaries will not allow contrast to area of injury = islands of dark signal in ocean of delayed enhancement.

Best seen on first pass imaging (25sec)

Independent factor of death and adverse LV remodelling. Zone of enhancement that extends from subendocardium toward the epicardium in a vascular distribution.

96
Q

Stunned myocardium:

Define it:

perfusion study?

contractility?

A

This is after an acute injury (ischaemia or reperfusion injury), dysfunction of myocardium persists even after restoration of the blood flow- can last days- weeks.

Perfusion study will be normal but contractility is crap.

97
Q

Hibernating myocardium Perfusion? contractility?

A

Chronic process , the result of severe CAD causing chronic hypoperfusion.

Decreased perfusion and decreased contractitility even when resting.

It is NOT an infarct. It is reversible with revascularisation.

98
Q

Scar:

A

This is DEAD myocardium. Will not squeeze normally and will have abnormal wall motion.

Revascularisation - NOT helpful.

99
Q

Hibernating myocardium on FDG PET?

A

On a FDG PET, this tissue will take up tracer more intensely than normal myocardium and will also show redistribution of thallium.

100
Q

Stunned vs hibernating vs scar:

A

Stunned: Associated with acute MI. - Normal perfusion. - Abnormal wall motion.

Hibernating: Associated with high grade CAD. - Abnormal perfusion. - Abnormal wall motion. - Will take up FDG and delayed thallium.

Scar: Associated with chronic prior MI. - Abnormal fixed perfusion - Abnormal wall motion. - No uptake with FDG or Thallium.

101
Q

How does delayed imaging work?

A
  1. Increased volume of contrast material distribution in acute MI
  2. Scarred myocardium washes out more slowly.
102
Q

How is delayed imaging performed?

A

By using IR to null normal myocardium followed by Gradient echo. T1 shortening from Gd looks bright. (Bright is Dead)

103
Q

What medications are used in stress imaging?

A
    • Dobutamine- inotropic stress agent for wall motion -
  • Adenosine - vasodilator for perfusion analysis.
104
Q

Is microvascular obstruction seen in chronic MI?

A

Microvascular obstruction is NOT seen in chronic MI as these will turn to scars eventually.

In acute settings: injured myocardium will have increased T2 signal which can be used to to estimate the area at increased risk, which can be used to estimate the area at risk (T2 bright enhanced = salvageable tissue)

105
Q

Acute vs chronic MI on MRI

A
  • Both have delayed enhancement - Acute will have normal thickness - T2 signal from oedema may be increased in the acute setting.
  • NO microvascular obstruction in chronic
  • ACUTE is T2 bright and CHRONIC (scar) is T2 Dark.
106
Q

Types of ventricular aneurysm:

A
  • True: Mouth is wider than body. Myocardium is intact. Usually on the anteriolateral wall.
  • False: Mouth is narrower than body. Myocardium is NOT intact (pericardial adhesions contain the rupture). Usually posteriolateral wall. Higher risk of rupture.
107
Q

How would you grade viability? Prognosis?

A

Based on % of transmural thickness involved in the thickness.

  • <25%: likely to improve with PCI -
  • 25-50%: may improve -
  • 50-100%: unlikely to recover function.
108
Q

What is the timing on the bad sequelae of an MI:

DRESSLER SYNDROME

A

4-6 weeks

109
Q

What is the timing on the bad sequelae of an MI:

Papillary muscle rupture

A

2-7 days

110
Q

What is the timing on the bad sequelae of an MI: Ventricular pseudoaneurysm

A

3-7 days

111
Q

What is the timing on the bad sequelae of an MI: Ventricular aneurysm

A

months- requires remodelling and thinning

112
Q

What is the timing on the bad sequelae of an MI: Myocardial rupture

A

Within 3 days (50% of the time).

113
Q

Where is the most common site affected by mets in the heart?

A

Pericardium. Pericardial effusion and pericardial lymph nodes

  • Melanoma may involve the myocardium
  • Lung cancer: epi/myocardium
114
Q

Most common primary malignant tumour of the heart:

A

Angiosarcoma

115
Q

Where does angiosarcoma affect?

A

RA and pericardium. They cause right sided heart failure and /or tamponade.

116
Q

Angiosarcoma appearance?

A

Bulky and heterogenous BUZZWORD: SUNRAY

117
Q

What are the left atrial myxoma associated with?

A

MEN syndrome and Blue Nevi (Carney complex)

118
Q

Where is LA myxoma usually located? appearance?

A

They are attached to interatrial septum. They may be calcified.They may prolapse through the MV. Will enhance with Gd- important discriminator against thrombus.

119
Q

Rhabdomyoma

A

Most common fetal cardiac tumour. Hamartoma. Prefer the LV.

Associated with Tuberous sclerosis.,

120
Q

Fibroma

A

2nd most common in paeds. IV septum Dark on T1 and T2 Enhance very brightly on perfusion and late Gd.

121
Q

Fibroelastoma

A

Most common neoplasm to involve the valve (80% aortic or mitral). Highly mobile on SSFP cine Systemic emboli are common- especially on the left side.

122
Q

Most common fetal cardiac tumour?

A

Rhabdomyoma.

123
Q

These cardiac tumours are associated with tuberous sclerosis:

A

Rhabdomyoma

124
Q

Most common cardiac tumour to involve the cardiac valves?

A

Fibroelastoma

125
Q

Systemic emboli are common with these tumours.

A

Fibroelastoma

126
Q

Define dilated cardiomyopathy:

A

This is dilatation with end diastolic diameter > 55mm and reduced EF.

127
Q

Causes of dilated cardiomyopathy: (5)

A
  1. Idiopathic- No enhancement or linear mid myocardial enhancement. 2. Ischaemic- Sunendocardial enhancement 3. Alcohol 4. Chagas 5. Cyclosporin
128
Q

What valvular pathology is dilated cardiomyopathy associated with?

A

MR

129
Q

What is Restrictive cardiomyopathy? What are the main 3 types?

A

This is anything that reduces the diastolic function. 1. Replacement by fibrosis: Endocardial fibroelastosis 2. Infiltration: Amyloidosis 3. Damage by Fe: Haemochromatosis.

130
Q

Typical appearance of amyloidosis on heart:

A

causes abnormal diastolic function: - biatrial enlargement - concentric thickening of the LV - Reduced systolic function of both ventricles.

131
Q

The inversion time is very long for this condition and it will be very difficult to suppress the myocardium.

A

Amyloidosis.

132
Q

In this confition, there will be bilateral ventricular thrombus:

A

Eosinophilic cardiomyopathy (Loeffler) Long TI is needed.

133
Q

Causes of constrictive pericarditis:

A
  1. TB/Viral 2. Iatrogenic secondary to CABG 3. Radiation.
134
Q

Signs associated with constrictive pericarditis:

A
  1. Calcification is diagnostic esp in the AV groove. 2. Pericardium is thickened > 4mm 3. Sigmoidisation on SSFP cine images: DIASTOLIC BOUNCE- more pronounced during inspiration.
135
Q

Re Myocarditis Define it: Distribution:

A

Inflammation of the heart. The late Gd follows a non vascular distribution preferring the lateral free wall. The pattern will be epicardial or mid wall and NOT subendicardial

136
Q

Re Cardiac Sarcoidosis Signal intensities. Parts affected

A

Signal in both T2 and early Gd will be increased Late Gd may be middle and epicardial in non coronary distribution. Often involves the septum. The RV and papillaries are rarely affected.

137
Q

DDx for cardiac sarcoidosis:

A

Focal wall thickening from oedema can mimic hypertrophic cardiomyopathy

138
Q

Takutsubo cardiomyopathy Def BUZZWORD

A

Transient akinesia of the LV apex without coronary stenosis. Ballooning of the LV apex is a buzzword. No delayed enhancement.

139
Q

Classic history for Takutsubo cardiomyopathy

A

chest pain with ECG changes in post menopausal women after : - break up - winning the lottery - some form of stress

140
Q

What is ARVC? - Which heart chamber affected? - Which ventricle is normal? - What MR sequence is useful?

A

It is Arrhymogenic Right Ventricular Cardiomyopathy - It is the fibrofatty degeneration of the RV leading to arrhythmia and sudden death. The LV is NORMAL. FAT SAT: FAT in RV

141
Q

What is hypertrophic cardiomyopathy?

A

Abnormal cardiomyopathy (from disarray of myofibrils) of the myocardium that affects diastole. one type is the asymmetric hypertrophy of IV septum- cause of sudden death.

142
Q

What are the imaging features of hypertrophic cardiomyopathy?

A

Patchy midway delayed enhancement of the hypertrophied muscle.

143
Q

What is non compaction cardiomyopathy?

A

It is as a result of loosely packed myocardium affecting the LV. The LV has a spongy appearance with increased trabeculation and deep intertrabecular recesses

144
Q

How would you diagnose non compaction cardiomyopathy?

A

Ratio of non compacted end diastolic myocardium to compacted end diastolic myocardium of more than 2.3:1

145
Q

Muscular dystrophy:

A

They have biventricular replacement of myocardium with connective tissue and fat (delayed Gd enhancement in the midwall). They often have dilated cardiomyopathy.

146
Q

What are the two main types of muscular dystrophy?

A

Becker ( Mild) Duchenne ( Severe) Both are X linked.

147
Q

BUZZWORD for Muscular dystrophy:

A

kid with dilated heart and midwall enhancement.

148
Q

Causes of pericardial effusion: (3)

A
  1. Lupus 2. Dressler’s syndrome - inflam effusion post MI 3. Uraemia
149
Q

What is the name of the sign seen on lateral CXR in pericardial effusion:

A

Oreo cookie sign- two lucent lines on CXR with a central opaque line (pericardial fluid)

150
Q

What are the two signs of cardiac tamponade?

A
  1. “short axis imaging during deep inspiration showing flattening or inversion of inter ventricular septum towards the LV, a consequence of augmented RV filling. 2. Reflux of contrast into the IVC and azygos system.
151
Q

A cystic mass lesion seen in the right cardiophrenic sulcus, separate from the pericardium. What is the lesion?

A

Pericardial cyst

152
Q

What part of the heart is affected in congenital absence of pericardium?

A

Partial absence of pericardium over the left atrium and adjacent pulmonary artery.

153
Q

What happens to the heart when there is left partial absence of pericardium?

A

The heart shifts to the LEFT. The heart could be contacting the left chest wall on CT/MR.

154
Q

What patients are at increased risk of cardiac volvulus/herniation?

A

Patient who undergo extra pleural pneumonectomy- herniation can only occur if the lung has also been removed.

155
Q

Which part is the most at risk to become strangulated?

A

The LEFT atrial appendage.

156
Q

With regard to imaging techniques in detection of hibernating myocardium, what method has the greatest specificity?

A

Dobutamine stress MRI is a good method for the assessment of myocardial hibernation- using a low dose protocol, and ischaemia (high dose protocol), MRI provides superior spatial resolution when compared with echo, and improvement in resting wall motion abnormality is considered a sign for myocardial hibernation.

chest FRCR (3 decks)

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