12

DAVID SUTTON

DAVID SUTTON PICTURES

DR. Muhammad Bin Zulfiqar PGR-FCPS III SIMS/SHL

• 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.

• 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

• 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).

• 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.

• 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.

• 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.

• 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.

• 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.

• 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).

• 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.

• 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.

• 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).

• 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

• 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.

• 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

• 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.

• 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.

• 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.

• 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

• 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.

• 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.

• 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.

• 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.

• 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.

• 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.

• 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).

• 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

• 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.

• 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.

• 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.

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

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

• 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.

• 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

• 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

• 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.

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

• 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.

• 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.

• 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.

• 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).

• 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.

• 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.

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.

• 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.

• 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

• 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.

• 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.

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

• 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.

• 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).

• 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.

• 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.

• 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.