DAVID SUTTON PICTURES Only for study purpose

1. 12
DAVID SUTTON

2. DAVID SUTTON PICTURES
DR. Muhammad Bin Zulfiqar
PGR-FCPS III SIMS/SHL

3. • Fig. 12.1 Non-contrast-enhanced CT scan of the
thorax. There is heavy calcification of the left
anterior descending coronary artery (arrows). I n
addition there is a hiatus hernia and calcification
of the pleurae indicating previous asbestos
exposure.

4. • Fig. 12.2 A 19 -technetium myocardial perfusion scan
showing SPECT images. This study is performed after
exercise stress of the myocardium (top images) and a
later study was performed at rest (bottom images). The
images are through the short axis of both the left and
right ventricle and demonstrate a partially reversible
perfusion defect in the interventricular septum and
posterior wall of the left ventricle

5. • Fig. 12.3 A transthoracic echocardiogram
demonstrating an apical four chamber view.
There is an aneurysm of the apex of the left
ventricle that has developed as a complication of
a previous myocardial infarction. Within the
aneurysm is a hyperechoic thrombus (arrow).

6. • Fig. 12.4 Left ventricular aneurysm. Contrast
enhancement demonstrates neck of apical and
posterior aneurysm communicating with left
ventricular cavity. This has the typical appearance
of a false aneurysm of the left ventricle.

7. • Fig. 12.5 Transthoracic echocardiogram showing a dilated
cardiomyopathy. The top 2D reference image shows the left
parasternal long-axis view and the lower panel shows the
corresponding M-mode trace. The left ventricle is markedly
dilated with a diastolic diameter of 8.1 cm and a systolic
diameter of 7.3 cm. There is poor contractility overall but
the posterior wall contracts slightly better than the septum.

8. • Fig. 12.6 Short-axis ECG-gated white blood MRI of the left ventricle in
diastole (A) and systole (B) in a patient with a dilated cardiomyopathy
performed at the level of the papillary muscles. The left ventricular
diameter in both phases of the cardiac cycle has been measured, allowing
calculation of the ejection fraction. The mean diastolic diameter was 6.7
cm and the mean systolic diameter was 5.9 cm. In addition the ventricular
wall thickness has been measured, increasing from a mean of 1.2 cm in
diastole to 1.45 cm in systole.

9. • Fig. 12.6 Short-axis ECG-gated white blood MRI of the left
ventricle in diastole (A) and systole (B) in a patient with a dilated
cardiomyopathy performed at the level of the papillary muscles.
The left ventricular diameter in both phases of the cardiac cycle has
been measured, allowing calculation of the ejection fraction. The
mean diastolic diameter was 6.7 cm and the mean systolic diameter
was 5.9 cm. In addition the ventricular wall thickness has been
measured, increasing from a mean of 1.2 cm in diastole to 1.45 cm
in systole.

10. • Fig. 12.7 A gradient-echo T 1 -weighted axial MRI
scan of the right ventricle. The right ventricular
wall contains fat, high signal on both T 1 - and T2
-weighting (arrow). This fatty replacement is
diagnostic of arrhythmogenic right ventricular
dysplasia.

11. • Fig. 12.8 An M-mode echocardiogram, showing systolic
anterior motion of the mitral valve apparatus (black
arrow). This abnormal motion of the valve apparatus is a
feature of hypertrophic obstructive cardiomyopathy caused
by the altered haemodynamics of the small ventricular
cavity and the prominent septum. The marked septal
hypertrophy contrasts with the almost normal thickness
posterior left ventricular wall (white arrows).

12. • Fig. 12.9 Apical four-chamber transthoracic
echocardiogram in a patient with hypertrophic
cardiomyopathy. (A) Septal hypertrophy (S) and systolic
anterior motion of the mitral valve (arrows). Image (B) is
taken from the same site in systole and shows the
generation of a high-velocity turbulent color flow Doppler
signal by the outflow tract obstruction. There is also
associated mitral regurgitation.

13. • Fig. 12.10 Apical continuous-wave Doppler trace in
a patient with dynamic left ventricular outflow
tract obstruction due to hypertrophic
cardiomyopathy. The curve has a characteristic late
systolic peak with a peak velocity of 5.6 m/s. This
indicates a peak instantaneous pressure drop at
this site of 125 mmHg.

14. • Fig. 12.11 Coronal gradient-echo MRI image
(ECG gated) through the left ventricular outflow
tract and aortic valve in a patient with calcific
aortic stenosis. There is calcification of the aortic
valve which produces a signal void (arrow).

15. • Fig. 12.12 Continuous-wave apical spectral Doppler
recording through the aortic valve in a patient with both
aortic stenosis and regurgitation. The peak velocity across
the valve in systole is 5.5 m/s (arrow), suggesting a peak
gradient of 120 mmHg as calculated by the simplified
Bernoulli

16. • Fig. 12.13 Both images show color flow Doppler
images taken in the parasternal long-axis view.
(A) A very small central regurgitant jet indicating
mild aortic regurgitation. (B) A much broader
based jet in a patient with severe aortic
regurgitation.

17. • Fig. 12.14 An echocardiogram
performed with the transducer
positioned in the suprasternal
notch with extension of the
patient's neck to demonstrate
the aortic arch. The sample
volume for pulsed-wave Doppler
interrogation has been
positioned in the descending
portion of the arch (arrow) (top)
and the Doppler spectral trace
illustrates normal forward flow
into the descending aorta in
systole and prominent reversal of
flow in diastole, due to the
presence of severe aortic
regurgitation. Many patients can
tolerate significant isolated aortic

18. • Fig. 12.15 A transoesophageal echocardiogram, at the
level of the left atrium, showing a four-chamber view of
the heart in a patient with mitral stenosis. The left atrium is
at the top of the image and contains spontaneous echo
formation due to the stagnation of flow in the distended
chamber. The thickened and restricted mitral leaflets are
indicated by arrows.

19. • Fig. 12.16 A transoesophageal echocardiogram, at the
level of the left atrium (arrows), showing a four-
chamber view of the heart. A color Doppler flow
examination through the mitral valve shows a small
mitral orifice size with acceleration of flow and
turbulence at the site of narrowing.

20. • Fig. 12.17 Continuous-wave Doppler examination of
the mitral valve from a transoesophageal echo
examination. The patient is in atrial flutter. The
diastolic flow into the left ventricle has a high peak
velocity of 1.8 m/s. The characteristic shape of the
curve shows only a slow diminution of flow velocity
during diastole. This trace can be used to calculate
pressure half time and estimate the mitral orifice area.

21. • Fig. 12.18 M-mode echocardiogram through
the aortic valve from a left parasternal
position. There is a massively enlarged left
atrium (arrow) with a

22. • Fig. 12.19 Transthoracic continuous-wave Doppler examination of
the mitral valve from the apex. The flow pattern of mixed mitral
valve disease is shown. The restricted forward ventricular filling
pattern of mitral stenosis is demonstrated, together with the large
regurgitant jet (arrow) which has a peak velocity of 5 m/s.

23. • Fig. 12.20 An apical long-axis view of the heart from a
transthoracic examination. (A) Prolapse of the anterior
mitral valve leaflet (arrow). Color flow Doppler
examination (B) taken from the same position shows
prominent eccentric regurgitant flow directed towards
the inferior wall of the dilated left atrium.

24. • Fig. 12.21 A transoesophageal long-axis
echocardiogram with color flow Doppler
examination that demonstrates clearly a
prominent jet of severe mitral regurgitation. The
green colors indicate 'variance' due to high-
velocity turbulence in the jet.

25. • Fig. 12.22 An apical four-chamber view from a transthoracic
examination in a patient with pulmonary hypertension. A color
flow (top) and continuous-wave Doppler examination of the
tricuspid valve is shown. The spectral trace demonstrates
regurgitation through the valve into the right atrium and
measurement of the flow velocity of the jet allows an assessment
of the right heart pressure. In this case the peak jet velocity of 4
m/s suggests an estimated right ventricular pressure of at least 70
mmHg.

26. • Fig. 12.23 Transoesophageal echocardiogram of a
patient with a bileaflet prosthetic mitral valve.
The two leaflets are shown open in diastole (A)
and closed in systole (B). Prominent ultrasonic
artefacts are generated from the prosthetic
material. LA = left atrium; LV = left ventricle; RA =
right atrium; RV = right ventricle.

27. • Fig. 12.24 Transoesophageal echocardiogram of a
patient with mitral stenosis and infective endocarditis
of the mitral valve. A small vegetation is seen
prolapsing into the left atrium in systole (arrow). LA =
left atrium; LV = left ventricle.

28. • Fig. 12.25 Transoesophageal echocardiogram in
the long-axis plane. The bicuspid aortic valve
shows large vegetations on opposing leaflets (A)
(arrow). The short axis view confirms the bicuspid
anatomy and shows the ' kissing' vegetations on
opposing leaflets (B) (arrow).

29. • Fig 12.26 Coronal gradient-echo MRI scan at
the level of the aortic valve in a patient with
aortic valve stenosis. The high-velocity
turbulent jet entering the aortic root is seen
as a signal void

30. • Fig. 12.27 Transthoracic echocardiogram in the
parasternal long-axis view showing a moderate
size pericardial effusion both anteriorly and
posteriorly. LV = left ventricle; LA = left atrium; RV
= right ventricle; Eff = pericardial effusion.

31. • Fig. 12.28 Transthoracic echocardiogram from
the apex showing diastolic collapse of the
right atrial free wall (arrows). LV = left
ventricle; LA = left atrium; RV = right
ventricle.

32. • Fig. 12.29 Transthoracic echocardiogram
demonstrating a large pericardial effusion (double-
headed arrow). This effusion is large enough to
compromise the cardiac output and a 6Fr pigtail
catheter (arrow) has been placed under ultrasound
guidance into the effusion to allow drainage.

33. • Fig. 12.30 Pericardial thickening (arrows) in a
patient in chronic renal failure.

34. • Fig. 12.31 Chronic constrictive pericarditis
with focal pericardial calcification (arrow).

35. • Fig. 12.32 Inflammatory pericarditis on transverse (A) and
parasagittal (B) ECG-gated T 1 -weighted spin-echo (SE
750/15) images following intravenous administration of
gadolinium chelate. There is a large low-signal pericardial
effusion (e) with marked enhancement of the parietal
(curved arrow) and visceral (straight arrow) pericardia.

36. • Fig. 12.33 I n the frontal chest radiograph (A) there is a convex abnormality of the
right heart border which is the classic appearance of a simple pericardial cyst.
The transthoracic echocardiogram (B) confirms the presence of a cyst adjacent to
the right atrium (arrows). A contrast-enhanced CT scan (C) confirms the presence
of a simple cyst, containing fluid of a low attenuation. This CT scan also
demonstrates fine calcification in the cyst wall, an uncommon feature

37. • Fig. 12.33 I n the frontal chest radiograph (A) there is a convex
abnormality of the right heart border which is the classic appearance of
a simple pericardial cyst. The transthoracic echocardiogram (B) confirms
the presence of a cyst adjacent to the right atrium (arrows). A contrast-
enhanced CT scan (C) confirms the presence of a simple cyst, containing
fluid of a low attenuation. This CT scan also demonstrates fine
calcification in the cyst wall, an uncommon feature

38. • Fig. 12.34 A non-contrast-enhanced CT of the heart.
There are multiple pericardial cysts of varying size
surrounding the heart in a patient with hydatid
disease. The attenuation value has been measured in
two of the cysts (0). The attenuation was less than 30
Hounsfield units, consistent with a simple cyst. Hydatid
disease is a rare cause of pericardial cysts.

39. • Fig. 12.35 Carcinoma of the bronchus
invading the left atrium (*), transgressing the
pericardium.

40. • Fig. 12.36 A transthoracic echocardiogram in
the parasternal long-axis view. An echogenic
mass can be identified prolapsing through the
mitral valve (arrow). This was an atrial
myxoma. LA = left atrium; LV = left ventricle;
RV = right ventricle; Ao = aortic root.

41. • Fig. 12.37 Two different echocardiograms in a patient with
an atrial myxoma. (A) A transthoracic apical four-chamber
view. The soft-tissue mass (arrow) is difficult to identify.
However, a transoesophageal examination (B) clearly shows
the tumour (arrow). Transoesophageal echocardiography is
the method of choice for visualising the posterior
structures of the heart.

42. • Fig. 12.38 Malignant angiosarcoma-CT scan
with contrast. The tumour mass appears as an
irregular filling defect in the right atrium and
ventricle. The left ventricle is displaced
posteriorly (arrows). A large pericardial
effusion surrounds the heart.

43. • Fig. 12.39 A contrast-enhanced CT scan in a
patient with non-Hodgkin's lymphoma. There is
a large soft-tissue defect filling the right atrium
(large arrow). This mass was biopsied and was
shown to be a lymphoma. In addition, a right-
sided pleural effusion has also developed (small
arrows).

44. • Fig. 12.40 Enhancing bronchial carcinoma (curved arrows)
invading the left lower lobe bronchus, left atrium and descending
aorta on a transverse gated TI-weighted post-gadolinium-DTPA spin-
echo image (TE 26 ms). Note the associated lower-lobe collapse,
which is difficult to differentiate from the tumour. The left coronary
artery (straight arrow), with its anterior descending and circumflex
branche , is shown. a = ascending aorta; d = descending aorta; la =
left atrium; p = pulmonary artery; s = superior vena cava.

45. • Fig. 12.41 A transoesophageal echocardiogram
of the descending aorta clearly identifies a
dissection flap present (arrows). This region is
poorly visualised by transthoracic
echocardiography because of its posterior
location.

46. Fig. 12.42 A contrast-enhanced CT scan of the
mediastinum at the level of the right pulmonary
artery. The ascending and descending aorta are both
heavily calcified and dilated. A dissection flap is clearly
visualised in both components of the aorta, with equal
contrast opacification in both the false and true lumen.
This is a Stanford type A dissection.

47. • Fig. 12.43 A contrast-enhanced CT scan of the mediastinum (A) at
the level of the right pulmonary artery. The timing of the scan
shows the maximum contrast opacification in the pulmonary
arteries but a dissection flap can be identified in both the ascending
and descending components of the aorta. In this patient with a
Stanford type A dissection the dissection extended into the
abdomen and involved the main right renal artery leading to renal
ischaemia (B). A small part of the kidney enhances supplied by an
accessory renal artery.

48. • Fig. 12.44 A gradient-echo axial MRI through a dilated descending
aorta using a white blood tine sequence. Several images are
obtained at this level over a period of time. Initially blood flowing
in the true lumen is white (arrow), indicating a previous dissection
(A). However, when the full sequence is assessed there is an
increase in the signal of a second false lumen on (B) (arrows). A
further lumen fails to opacity. This suggests there are three
components to this chronic dissection

49. • Fig. 12.45 Contrast-enhanced CT scan of the
lower descending aorta demonstrating a
penetrating ulcer (arrow), which has ruptured
into the para-aortic space. This ulcer has
developed as a result of atherosclerotic
disease.

50. • Fig. 12.46 Contrast-enhanced CT scan of a young man who
was involved in a high-speed road traffic accident. There is a
small mediastinal collection and a left-sided pleural effusion
(white arrows). In addition a small defect can be identified in
the lumen of the descending aorta (black arrow). This small
defect represents d transection of this vessel, which was
confirmed on angiography.

51. • Fig. 12.47 Aortic angiogram in the left
anterior oblique view. This shows aortic
transection with localised extravasation and a
left pleural effusion.

52. • Fig. 12.48 Contrast enhanced CT pulmonary
angiogram demonstrating a large filling defect
in an enlarged left lower lobe pulmonary
artery (arrow). This is a large proximal
pulmonary embolism.

53. • Fig. 12.49 This contrast enhanced CT pulmonary
angiogram identifies additional features that can
be detected on CT and supports the diagnosis of
pulmonary embolism. There is a right-sided
pleural effusion and dilatation of the right
ventricle (arrow).

54. • Fig. 12.50 Pulmonary angiogram showing a small
embolus in the right lower lobe artery (arrow).
Angiography remains the most sensitive method
of identifying small subsegmental pulmonary
emboli.

55. • Fig. 12.51 Normal perfusion (A) and
ventilation (B) scans in the posterior
projection. There are no significant differences
in appearances and there is no evidence of
pulmonary embolus.

56. • Fig. 12.52 Abnormal perfusion (A) scan and
normal ventilation (B) scan in the posterior
projection. There are multiple perfusion
defects in both lungs that are not matched by
ventilation defects.