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The heart and great vessels

image of The heart and great vessels
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Abstract

This chapter summarizes an overview of techniques utilized in the diagnosis and assessment of various cardiovascular diseases. It outlines normal cardiac anatomy and radiographic features, congenital defects, acquired valvular diseases, myocardial diseases, pericardial effusions, parasitic infections and vascular disorders. Additionally, spectral Doppler echocardiography principles are covered for the estimation of chamber pressures and shunt calculation.

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Figures

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9.1 Cardiac position as seen on a DV radiograph. Variation in position may be a normal variant or a congenital abnormality. Some of the reported congenital abnormalities are included; many other variants are possible. Ao = aorta; Ap = apex; ST = stomach. (Line diagrams adapted from Suter (1984) with permission)
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9.2 Dextroposition identified as an incidental finding in a dog. The cardiac silhouette and apex are located to the right of the median plane and there is no evidence to suggest that this is associated with a mediastinal shift. Note the aorta (arrowed) and stomach (St) are on the left; there is no suggestion of a situs inversus in this dog.
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9.3 Left ventricular angiocardiograms of a 5-year-old Golden Retriever. (a) The catheter has been placed into the LV via the femoral artery and aorta ready for the contrast medium injection. (b) Positive contrast medium fills the LV, ascending aorta (Ao), brachiocephalic trunk (B) and left subclavian artery (S), and surrounds the aortic valves (arrowed). (Courtesy of J. Buchanan)
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9.4 Right ventricular angiocardiograms of the same dog as in Figure 9.3 . (a) The catheter has been placed into the RV via the caudal vena cava ready for the contrast medium injection. (b) Positive contrast medium is present within the RV and has started to enter the right ventricular outflow tract and pulmonic trunk (MPA). (c) The contrast medium has now reached the left and right pulmonary arteries (arrowed) and the smaller pulmonary arterial branches in the lungs. (Courtesy of J. Buchanan)
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9.5 Location of the cardiac chambers on thoracic radiographs of a dog. (a) Lateral view. (b) VD view. Ao = aortic arch; BR = brachiocephalic trunk; CdVC = caudal vena cava; CrVC = cranial vena cava; IT = internal thoracic arteries and veins; LAA = left atrial appendage; LPA = left pulmonary artery; LS = left subclavian artery; MPA = pulmonic trunk; RAA = right atrial appendage; RPA = right pulmonary artery. (Reproduced from with permission)
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9.6 Location of the cardiac chambers on thoracic radiographs of a cat. (a) Lateral view. (b) VD view. Ao = aortic arch; CdVC = caudal vena cava; CrVC = cranial vena cava; LAA = left atrial appendage; MPA = pulmonic trunk; RAA = right atrial appendage. (Reproduced from with permission)
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9.7 Clock face analogy identifying location of cardiac chambers. (a) Lateral view. (b) DV view. Ao = aortic arch; LAA = left atrial appendage; MPA = pulmonic trunk; RAA = right atrial appendage. (Reproduced from with permission)
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9.8 (a) Lateral radiograph of a cat with a normal cardiac silhouette. The cardiac silhouette is ovoid. Alteration in cardiac shape is useful in radiographic diagnosis of cardiac disease in the cat. (b) DV thoracic radiograph of a cat with a normal cardiac silhouette. The cardiac silhouette is ovoid. Alteration in cardiac shape is useful in radiographic diagnosis of cardiac disease in the cat.
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9.10 (ai) Right lateral and (aii) DV thoracic radiographs from a Golden Retriever with a normal heart confirmed by echocardiography. The lateral view shows a large amount of sternal contact (common in the breed and conformation type), but the DV view excludes right-sided cardiomegaly and the cardiac silhouette is within normal limits. (bi) Right lateral and (bii) DV thoracic radiographs from a Dobermann with a normal heart confirmed by echocardiography. As is usual for the Dobermann’s conformation, the heart is vertical within the thorax on the lateral view, and therefore appears small craniocaudally on the DV view with the apex still left-sided. Volume depletion can be seen, with a slightly small cardiac silhouette and slender CdVC. Pericardial fat is also visible on the lateral view, ventral to the cardiac silhouette.
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9.11 DV thoracic radiograph of an obese Domestic Shorthaired cat. The cardiac silhouette has an unusual shape due to border effacement with a triangular soft tissue opacity on the right side (arrowed). A CT examination confirmed the lung was within normal limits and the opacity was due to a large amount of pericardial fat (even though it has a soft tissue opacity). This appearance should not be confused with pathology.
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9.12 Left lateral thoracic radiograph of a clinically normal 12-year-old cat. In about 40% of older cats the heart has a more horizontal, cranially sloping position.
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9.14 VD thoracic radiographs of a Cavalier King Charles Spaniel with cardiomegaly, obtained at different phases of the cardiac cycle. Note the difference in the appearance of the heart. (a) Systole: the ventricles are smaller and the atria are dilated (arrowed). (b) Diastole: the entire heart is rounded and the atrial bulges are not as prominent. The changes in this dog are also exacerbated by slight differences in respiratory phase.
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9.15 Technique to perform a VHS on a left lateral thoracic radio- graph of a 6-year-old Labrador Retriever. First draw the long axis of the heart (L), connecting the ventral margin of the left stem bronchus at the carina with the ventral contour of the cardiac apex. Then draw the maximal short axis (S) of the dorsal third of the heart (at or above the level of the caudal vena cava) perpendicular to the long axis. Transpose both measurements on to the vertebral column, starting at the cranial endplate of the 4th thoracic vertebra. Count and add the number of vertebrae covered by both measurements. In this example L = 5.6 vertebrae and S = 4.6 vertebrae, giving the dog a VHS of 10.2 vertebrae, which is within the normal range for the breed (10.2–11.4). Both lateral views can be used for the VHS, but on the left lateral view, the left principal bronchus is more ventral than the right principal bronchus (arrowed), making it easier to determine the dorsal landmark for the L measurement.
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9.17 Determining the VLAS. To calculate the VLAS, draw a line from the carina to the caudal vena cava and compare the length of that line to the vertebral column. See text for measurement details. (a) Lateral thoracic radiograph of a normal Boxer with a VLAS of approximately 2.2. (b) Lateral thoracic radiograph of an Airedale Terrier with stage B2 myxomatous mitral valve disease (MMVD) and a VLAS of approximately 2.6. (c) Lateral thoracic radiograph of a Jack Russell Terrier with advanced MMVD with congestive heart failure and a VLAS of 4.
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9.18 Basic principles of tracheal and bronchial displacement on lateral radiographs. The positions of the trachea, carina and principal bronchi can be very useful to assess cardiac chamber enlargement. Note that there is also variation in tracheal position between different dog breeds. (a) Normal. The trachea and principal bronchi have a gentle ventral divergence from the thoracic vertebral column. Note the slight ventral concavity (arrowed) in the trachea just cranial to the carina. (b) Left ventricular enlargement in isolation. When it is enlarged, the LV displaces the entire trachea dorsally and there is loss of the normal ventral bend cranial to the carina. (c) Left atrial enlargement in isolation. The LA creates a triangular or wedge-shaped soft tissue opacity at the caudal border of the cardiac silhouette and pushes the left principal bronchus (shown in dark blue) dorsally. (d) Cranial mediastinal mass. A cranial mediastinal mass (shown in pink) can elevate the trachea cranial to the carina anywhere along its length. Depending on the size and location of the mass, this may be focal elevation or, more commonly, elevation of the entire thoracic trachea with a pivotal point of the elevation over the mass. The cardiac size will be normal. (e) Right atrial enlargement or right atrial mass in isolation. It is very rare to see severe focal right atrial enlargement. An enlarged RA can focally dorsally deviate the trachea cranial to the carina (note that a heart base mass can also elevate the trachea in this position but usually has a different appearance on DV and VD views; see ‘Cardiac neoplasia’, below). Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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9.19 Close-up of a lateral thoracic radiograph of a dog demonstrating the normal appearance of the caudal trachea. Note the normal ventral bend (arrowhead) cranial to the carina, and the two principal bronchi almost level with one another (arrows point to their dorsal margins).
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9.20 (a) Close-up of a DV thoracic radiograph of a normal dog at the level of the heart. The bronchial tree is outlined. The angle between the left and right principal bronchi (arrowed) should be about 60 degrees and form an upside-down V shape. This does vary somewhat with breed, but an increased angle or splayed appearance (‘cowboy legs’ sign) suggests left atrial or tracheobronchial lymph node enlargement. (b) Postmortem bronchogram showing the normal angle between the principal bronchi. (Courtesy of B. Hopper)
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9.21 (a) Lateral thoracic radiograph of a cat with a small volume of pleural fluid associated with feline leukaemia virus infection. A narrow radiolucent line is visible in a position compatible with the cranial aspect of the heart (arrowed). Together with the position of the trachea and the caudal aspect of the cardiac silhouette, this line has the effect of completing a cardiac silhouette of normal appearance. (b) Lateral thoracic radiograph of a different cat with a larger volume of pleural fluid. In this instance, the position and size of the pericardial fat stripe, relative to the position of the trachea, suggests enlargement of the cardiac silhouette. Ultrasonography subsequently confirmed marked hypertrophic cardiomyopathy (and ruled out a mediastinal mass). (Reproduced from Lamb (2000) with permission)
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9.22 (a) Lateral and (b) DV thoracic radiographs of a dog showing the normal location and appearance of the aorta (arrowed in (a); black line in (b)).
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9.23 Lateral thoracic radiograph of an aged cat. Note the focal bulge in the aorta (arrowed).
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9.24 Close-ups of (a) lateral and (b) DV thoracic radiographs of a dog showing the normal size and location of the CdVC (lines in (a); arrows in (b)).
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9.25 Close-up of a lateral thoracic radiograph of a dog with a severe pneumomediastinum after trauma. The azygos vein (Az) is visible as a narrow tube of soft tissue opacity ventral to the vertebral column and dorsal to the aorta (Ao), connecting with vessels from each intercostal space (arrowed).
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9.26 VD thoracic radiograph of a normal dog. The pulmonic trunk appears as a small focal bulge at the 1–2 o’clock location (arrowed). This can be a normal finding on a VD view, or when an exposure is made during systole, and should not be interpreted as disease.
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9.27 Close-up of a lateral radiograph of a dog showing a cranial lobar pulmonary artery (white arrows) and vein (black arrows). At the point where they cross the third or fourth rib (blue arrow), these vessels (red arrows) should be no wider than the narrowest part of the rib.
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9.28 Close-up of a DV thoracic radiograph of a dog showing the right caudal lobar pulmonary artery (white arrows) and vein (black arrows) as they cross the eighth and ninth ribs. The vessels are measured where they cross the ninth rib. Blue arrows = rib measurements; red arrows = vessel measurements.
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9.29 Lateral thoracic radiograph of a dog with Addison’s disease (hypoadrenocorticism). The dog has microcardia. Note the narrow pointed appearance of the cardiac silhouette.
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9.30 Lateral thoracic radiograph of an extremely dehydrated dog. The CdVC is narrow (arrowed), the lungs are hyperlucent, and the cardiac silhouette is small and pointed.
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9.31 (a) DV and (b) right lateral thoracic radiographs of a 7-month-old Old English Sheepdog with tricuspid dysplasia. Right atrial enlargement can be seen on both views (arrowed). The RV is also volume overloaded with this condition, which affects the cardiac silhouette. (a) The DV view shows slight rotation, so the cranial mediastinum is projected to the left side.
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9.32 Thoracic radiographs of a 1.5-year-old Shih Tzu diagnosed with pulmonic stenosis. (a) The DV view shows a reversed-D-shaped cardiac silhouette, typical of right ventricular enlargement (arrowed). (b) The lateral view shows increased sternal contact with pericardial fat confirming mild apex tipping, consistent with right ventricular enlargement and concentric hypertrophy (arrowed). Both views show an enlarged pulmonic trunk (*). The lateral view is rotated, but still of diagnostic quality. (c) On the DV view, a line is drawn through the cardiac silhouette from the right side of the mediastinum to the cardiac apex; the right:left ratio of the cardiac silhouette is >1:1, consistent with right heart enlargement (normal is approximately 1:1). (d) On the lateral view, a line is drawn from the carina to the apex; the cranial:caudal ratio of the cardiac silhouette is >2:1, consistent with right heart enlargement (normal is approximately 2:1).
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9.33 Thoracic radiographs of a Lancashire Heeler with advanced MMVD and CHF. (a) Right lateral view showing significant left atrial enlargement tenting from the caudodorsal border of the cardiac silhouette (green shading). There is marked tracheal elevation; concurrent left ventricular enlargement contributes to the increased height of the cardiac silhouette. The principal bronchi are divided by the left atrial enlargement, elevating the left caudal lobar bronchus by a greater extent than the right bronchus. (b) DV view. The lateral deviation of the caudal lobar bronchi giving the cowboy leg sign is seen (black line = medial walls). The double opacity sign is evident (arrowed), showing the enlarged LA as a positive summation shadow on the cardiac silhouette. The LA extends to the LAA, projecting beyond the cardiac silhouette at 2–3 o’clock (arrowhead).
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9.34 (a) Lateral and (b) DV thoracic radiographs of a Dobermann with dilated cardiomyopathy and CHF. Note that left atrial enlargement is often the most prominent feature of the cardiac silhouette in this breed. Because of the very vertical heart in the normal Dobermann, left atrial enlargement can result in the LA being the most caudal part of the cardiac silhouette; as evident on the DV view. (a) The lateral view shows tracheal elevation and left atrial tenting. (b) This is difficult to see on the DV view as the left ventricular apex summates with the LA.
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9.35 (a) Lateral and (b) DV thoracic radiographs of a cat with HCM that is receiving treatment for CHF (controlled). (a) The lateral view does not clearly identify the left atrial enlargement. There is increased sternal contact, but echocardiography showed only left ventricular enlargement (concentric hypertrophy) and no right heart enlargement. (b) The DV view shows apparent biatrial enlargement, resulting in the ‘valentine heart’ shaped cardiac silhouette. Echocardiography did not identify right atrial enlargement; marked left atrial enlargement can result in the interatrial septum and right atrial wall being displaced to the right.
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9.36 Thoracic radiographs of a Cavalier King Charles Spaniel that is receiving treatment for advanced MMVD and CHF. (a) The DV view shows the left ventricular apex is shifted to the right, which is associated with left ventricular enlargement. The very enlarged LA can be seen, resulting in double opacity, and the caudal lobar bronchi can be seen as a cowboy leg appearance. (b) The lateral view shows a very tall cardiac silhouette, resulting in severe dorsal displacement of the caudal trachea. This is due to both left atrial and left ventricular enlargement.
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9.37 (a) Lateral and (b) DV thoracic radiographs of a middle-aged crossbreed dog with generalized cardiomegaly, secondary to MMVD.
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9.38 Thoracic radiographs of a 12-year-old terrier cross with a long-standing heart murmur that suffered an episode of collapse and then presented in cardiogenic shock. Both the (a) lateral and (b) DV views show a globoid cardiac silhouette with a static outline (most evident on the DV view). The dog had advanced MMVD but no overt CHF. Pericardial effusion was present and was believed to be due to a left atrial tear, as the LA was very dilated on echocardiography. The LA can be seen on the lateral view. Most cases of pericardial effusion do not show any radiographic evidence of specific chamber enlargement, but when the LA is very dilated (as detected by echocardiography), left atrial rupture must be considered as a cause.
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9.39 Lateral thoracic radiograph of a dog with subaortic stenosis. The entire aortic arch is enlarged (arrowed). This was confirmed on the DV view.
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9.40 Incidental aortic calcification identified on a lateral thoracic radiograph of a 10-year-old Weimaraner. The calcification is seen as a wavy opaque line over the cranial border of the cardiac silhouette (arrowed).
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9.41 (a) DV and (b) lateral thoracic radiographs of a dog with pulmonic stenosis and heartworm disease. (a) The enlarged pulmonic trunk can be seen as a bulge at the 1–2 o’clock position (arrowed). (b) The pulmonic trunk may mimic a nodule on the lateral radiograph when an end-on view is obtained (arrowed). This may occasionally occur in normal dogs or, as in this case, when the pulmonic trunk is enlarged. The lateral radiograph is slightly rotated.
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9.42 Pulmonary arterial and venous enlargement. The pulmonary artery and vein measurements are shown by arrows and the rib number is also shown. (a) Moderately enlarged cranial lobar pulmonary veins on a close-up of a lateral radiograph of a dog with heart failure. (b) Severely enlarged right caudal lobar pulmonary artery on a DV view of a dog with heartworm disease.
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9.44 Thoracic radiographs of a Jack Russell Terrier with advanced MMVD and left-sided CHF. (a) The lateral view shows marked, mainly left-sided cardiomegaly with tracheal elevation. The caudodorsal border of the cardiac silhouette cannot be easily seen because of the presence of a parenchymal opacification (mixed interstitial–alveolar pulmonary infiltrate). (b) The DV view shows generalized cardiomegaly and reveals that the parenchymal opacification is mainly right sided and consolidated (alveolar pattern) with air bronchograms. The pulmonary vasculature cannot be reliably assessed from either view because of the lung pattern.
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9.45 Thoracic radiographs of a Cocker Spaniel with dilated cardiomyopathy, following initial diuretic treatment. (a) The right lateral view shows generalized cardiomegaly and a mild residual interstitial lung pattern, which is mainly perihilar. The cranial lobar pulmonary vessels are within normal limits. Thoracic radiographs of a Cocker Spaniel with dilated cardiomyopathy, following initial diuretic treatment. (b) The DV view confirms mainly left-sided cardiomegaly. The caudal lobar pulmonary arteries and veins are both increased in size compared with the ninth rib (R9) as they cross it (the left-sided vessels are more easily assessed). White lines = pulmonary artery; black lines = pulmonary vein.
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9.46 (a) Lateral and (b) DV thoracic radiographs of a cat with HCM and left-sided CHF. Both views show a patchy interstitial pattern. (b) The DV view shows the beginnings of an alveolar pattern in the right lung.
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9.47 Thoracic radiographs obtained 24 hours after drainage of a pleural effusion in a cat with end-stage cardiomyopathy and severe left-sided CHF. (a) The lateral view shows severe ventral lung consolidation (alveolar pattern) with air bronchograms and partial border effacement of the cardiac silhouette and diaphragm. Thoracic radiographs obtained 24 hours after drainage of a pleural effusion in a cat with end-stage cardiomyopathy and severe left-sided CHF. (b) On the DV view, this makes it difficult to define the cardiac silhouette.
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9.48 Thoracic radiographs of a dog with right-sided heart failure. (a) Lateral view. A large volume of pleural effusion is present, obscuring the cardiac silhouette. The dog also has ascites and an enlarged liver (not seen on these radiographs). It is not possible to identify the cause of the effusion from these radiographs and further work-up would be required to confirm right-sided heart failure. Thoracic radiographs of a dog with right-sided heart failure. (b) DV view. A large volume of pleural effusion is present, obscuring the cardiac silhouette. The dog also has ascites and an enlarged liver (not seen on these radiographs). An enlarged right pulmonary caudal lobar vein (arrowed) suggests that pulmonary venous congestion may also be present due to left-sided heart disease. It is not possible to identify the cause of the effusion from these radiographs and further work-up would be required to confirm right-sided heart failure.
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9.50 Thoracic radiographs of a 1-year-old German Shepherd Dog bitch with left-sided CHF, myocardial failure and atrial fibrillation, subsequently diagnosed with a PDA. (ai) DV and (aii) right lateral views obtained at presentation. The dog was severely dyspnoeic and radiographs showed severe, generalized cardiomegaly, especially affecting the left side. There is a mixed interstitial and alveolar lung pattern, most marked in the perihilar and caudodorsal lung fields, consistent with cardiogenic pulmonary oedema. Pulmonary vasculature is difficult to assess given the lung pattern, but the left caudal lobar artery is enlarged. (bi) DV and (bii) right lateral views of the same dog after receiving CHF medication for three days, with almost complete resolution of the lung pattern. There is severe left atrial and left ventricular enlargement, and the aortic arch, pulmonic trunk and LAA are all prominent, giving the ‘triple knuckle’ appearance between 1 and 3 o’clock on the DV view. The right caudal lobar pulmonary artery is enlarged on the DV view and the cranial lobar vessels, especially the pulmonary vein, are enlarged on the lateral view. Thoracic radiographs of a 1-year-old German Shepherd Dog bitch with left-sided CHF, myocardial failure and atrial fibrillation, subsequently diagnosed with a PDA. (c) Same image as (bi), with the aorta marked in red, pulmonic trunk in blue and LAA in yellow to illustrate the triple knuckle appearance between 1 and 3 o’clock. (di) DV and (dii) right lateral views of the same dog on day 12, following placement of an ACDO (arrowed) to close the PDA. This was placed using cardiac catheterization of the descending aorta via the right femoral artery.
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9.51 (ai) 2D and (aii) colour flow Doppler images from a dog with a PDA. This is a cranial left parasternal view optimizing alignment with the pulmonic trunk (PA), beyond the pulmonic valves (PV). The PDA can be seen entering the pulmonic trunk prior to its bifurcation. (aii) The colour flow Doppler shows laminar flow in the ductus (red) which becomes turbulent after crossing the narrow pulmonary ostium of the PDA and flowing into the pulmonic trunk. This is a systolic frame, so pulmonary outflow can also be seen (blue). (b) Continuous wave Doppler of PDA flow, with the cursor aligned with flow. High-velocity flow is consistent with a normal aorta–pulmonic trunk pressure gradient (excluding significant pulmonary hypertension).
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9.52 (a) 2D and (b) colour flow Doppler intraprocedural transoesophageal echocardiographic images, prior to placement of an ACDO to close a left-to-right shunting PDA. The PDA narrows to a pulmonary ostium as flow enters the distal pulmonic trunk (PA). Flow in the PA during systole is red, as it is travelling towards the probe, from the right ventricular outflow tract (RVOT). PV = pulmonic valves.
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9.53 Still frame from a video-recorded angiocardiogram in a dog with a PDA. The pigtail catheter, delivered via the femoral artery, is in the descending aorta (Desc Ao), although it cannot easily be seen once the aorta is opacifed with contrast material. Its pigtail tip is positioned near the PDA, so contrast material can be seen within the PDA and opacifying the pulmonic trunk (PA) and left and right pulmonary arteries. There is minimal contrast enhancement of the aortic arch (AoA). The morphology is consistent with a type IIB PDA. This study preceded subsequent ACDO closure of the ductus.
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9.54 (a) DV and (b) right lateral thoracic radiographs of a 9-month-old male Border Terrier with an rPDA associated with pulmonary hypertension. The right heart is enlarged. An aortic bulge (‘ductus bump’) is evident on the DV view. The lung field is hypovascular.
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9.55 (a) Right parasternal long-axis four-chamber view and (b) short-axis view at the level of the papillary muscle in the same Border Terrier as in Figure 9.54. There is marked concentric hypertrophy of the RV resulting in flattening of the IVS. The pulmonic trunk was dilated with no evidence of pulmonic stenosis. Bidirectional flow was evident in a tubular ductus.
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9.56 Toy Poodle with pulmonary hypertension and bidirectional flow across the PDA. (a) Cranial left parasternal view of the pulmonic trunk and PDA in (ai) a diastolic frame showing some left-to-right flow and (aii) a systolic frame showing right-to-left flow across the ductus. (b) Spectral Doppler study of the PDA flow. The brief right-to-left flow (below baseline) and more prolonged left-to-right flow during diastole (above baseline) confirms bidirectional shunting and similar pulmonary arterial and systemic pressures (the PDA velocities are low). PA = pulmonic trunk.
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9.57 Angiocardiogram of a dog demonstrating a right-to-left shunt through a PDA in a case where significant pulmonary hypertension was present. The contrast medium was injected in the RV, and the aorta (Ao) is opacified at the same time as the pulmonic trunk (MPA). The region of the PDA is indicated by the arrow. (Courtesy of J. Buchanan)
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9.58 Labrador Retriever with type A valvular pulmonic stenosis. Right parasternal short-axis views optimizing the right ventricular outflow tract (RVOT) to plumonic trunk (PA). The pulmonic valve leaflets are thick and fused. (a) ‘windsock’ appearance during diastole. (b) domed appearance during systole.
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9.59 Normal coronary artery distribution in dogs and humans, and common patterns of single right coronary artery in the latter. In the type R1 pattern, the right coronary artery (RCA) continues as a single vessel and crosses the caudal crux of the atrioventricular sulcus (open arrow), then continues as the left circumflex (LCx) and left caudal descending (LCD) arteries. In type 2 patterns, the single vessel branches shortly after leaving the aorta. Sub-classifications are made depending on whether the crossing vessel (solid arrow) passes cranial to the pulmonic trunk (PT) (R2A), between the aorta and pulmonic trunk (R2B) or caudal to the aorta (R2C). (Reproduced from with permission)
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9.60 Bulldog diagnosed with severe pulmonic stenosis complicated by an aberrant coronary artery. Cranial left parasternal view optimized for the large, single coronary artery (arrowed) that encircles the RVOT immediately below the pulmonic valves, which were also abnormal (not shown). Oblique view of the pulmonic trunk (PA).
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9.61 (a) Right lateral and (b) DV thoracic radiographs of a Labrador Retriever cross with pulmonic stenosis. The increased sternal contact and ‘reversed D’ on the DV view support right ventricular enlargement. The apex tipping on the lateral view (arrowhead) supports right ventricular hypertrophy pushing the left ventricular apex dorsally. The post-stenotic dilatation of the pulmonic trunk (arrowed) is shown as a ‘pulmonic cap’ overlying the ventral trachea on the lateral view, and as a 1–2 o’clock bulge on the DV view.
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9.62 French Bulldog with pulmonic stenosis. (a) Right parasternal long-axis four-chamber view and (b) short-axis view at the level of the papillary muscles. Both views show an enlarged right heart, with concentric hypertrophy of the right ventricular wall (thicker than the LVFW). The pressure overload in the RV has resulted in flattening of the IVS, apparent in both views.
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9.63 Lhasa Apso with pulmonic stenosis. (a) Right parasternal long-axis four-chamber view. Note the right ventricular hypertrophy and the right atrial enlargement. (b) Right parasternal short-axis view at the level of the papillary muscles. The RVFW is severely thickened and the IVS is flattened. (c) M-mode echocardiogram acquired from the level shown in (b). Paradoxical motion of the IVS is present. (© J. Dukes-McEwan)
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9.64 Right parasternal short-axis view of the same French Bulldog as in Figure 9.62, optimizing the RVOT and pulmonic trunk (PA). The pulmonic valves (PV) were thickened and dysplastic, but the greatest site of obstruction was a supravalvular lesion.
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9.65 A young Chow Chow with a double-chambered RV. Right parasternal short-axis view showing the RA, RVOT, pulmonic valves (PV) and pulmonic trunk (PA). This case showed a complex muscular obstruction in the RVOT. This separated the inflow part of the RV (high pressure; associated with concentric right ventricular hypertrophy) from a lower pressure chamber of the RVOT between the obstruction and the pulmonic valve. This lesion resulted in RVOT obstruction. In addition, there was a VSD with right-to-left shunting across it. The aorta (Ao) is wide, and the pulmonic trunk is relatively small in comparison.
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9.66 Cocker Spaniel with valvular pulmonic stenosis (type A). Cranial right parasternal short-axis view with colour flow Doppler showing normal laminar flow in the RVOT, which suddenly develops colour variance reflecting turbulent flow with increased velocity beyond the pulmonic valves (PV) in the pulmonic trunk. TV = tricuspid valve.
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9.67 French Bulldog with pulmonic stenosis. Continuous wave Doppler obtained from a cranial right parasternal view optimized for the RVOT and pulmonic trunk. Peak velocity is over 6 m/s, consistent with very severe pulmonic stenosis. There is also a late-accelerating envelope, which corresponds to concurrent dynamic RVOT obstruction as a consequence of severe right ventricular hypertrophy (an indication for beta-blockers).
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9.68 Angiocardiograms after injection of contrast medium in the RV of a West Highland White Terrier with pulmonic stenosis. Both views show a catheter and fair to good opacification of the RV, RVOT, pulmonic trunk and pulmonary arteries. (a) On the lateral view, there is a clear narrowing at the level of the infundibulum as well as post-stenotic dilatation of the pulmonic trunk. (b) The VD view shows post-stenotic dilatation of the pulmonic trunk. (Courtesy of J. Buchanan)
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9.69 Still frame right-sided angiocardiogram of a Bulldog with pulmonic stenosis. Cranial is to the right of the image. Catheterization of the right side of the heart was performed via the right jugular vein. A pigtail catheter delivered contrast into the right ventricular apex. Very thick pulmonic valves (PV) can be seen, with little contrast filling at the level of the valves, suggestive of severe narrowing. The severe right ventricular hypertrophy is seen as soft tissue between the contrast material in the RV and the cranioventral border of the cardiac silhouette. There also appears to be some dynamic RVOT obstruction (between the two black arrows). The pulmonic trunk and lobar pulmonary arteries are dilated, consistent with post-stenotic dilatation.
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9.70 Still frame aortic root angiogram from the same dog as in Figure 9.69, with pulmonic stenosis but normal coronary arteries. Cranial is to right of the image. The aortic root has been catheterized via a femoral artery. The pigtail catheter is at the level of the aortic valves. There is contrast enhancement of the aortic root, brachiocephalic trunk (BCT), left subclavian artery (LSA), right coronary artery (RCA) and left circumflex branch (L Circ) of the left coronary artery. The sequence of contrast enhancement confirmed that both coronary arteries arose independently from the aortic root. There is mild blushing of contrast in the LV (aortic regurgitation caused by the presence of the catheter). A temperature probe in the oesophagus and leads associated with transthoracic defibrillation/pacing patches can also be seen. Desc Ao = descending aorta.
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9.71 Angiocardiogram in a Bulldog with pulmonic stenosis. The contrast medium was injected in the left ventricular outflow tract to opacify the aorta and the coronary arteries. A single coronary artery (arrowed) is seen, which then branches into right and left coronary arteries. (Courtesy of J. Buchanan)
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9.72 (a) Transverse, (b) sagittal and (c) dorsal multiplanar reformatted contrast-enhanced thoracic CT images (soft tissue reconstruction) of a Bulldog with confirmed valvular pulmonic stenosis. The aberrant course of the left coronary artery (arrowed) cranial to the pulmonic trunk (prior to branching into paraconal interventricular and left circumflex branches) is consistent with an R2A coronary artery abnormality. (Courtesy of Will Humphreys, University of Liverpool)
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9.73 (a) Transverse and (b) dorsal reformatted contrast-enhanced thoracic CT images (soft tissue reconstruction) of a 10-month-old French Bulldog with supravalvular pulmonic stenosis (the pulmonic valve did not appear to be contributing to the obstruction). The focal circumferential narrowing and interruption of the contrast column within the pulmonic trunk (arrowed) is consistent with pulmonic stenosis or segmental hypoplasia of the pulmonic trunk. The coronary artery anatomy in this dog was within normal limits. (c) Sagittal multiplanar reformatted contrastenhanced thoracic CT images (soft tissue reconstruction) of a 10-month-old French Bulldog with supravalvular pulmonic stenosis (the pulmonic valve did not appear to be contributing to the obstruction). The focal circumferential narrowing and interruption of the contrast column within the pulmonic trunk (arrowed) is consistent with pulmonic stenosis or segmental hypoplasia of the pulmonic trunk. The coronary artery anatomy in this dog was within normal limits. (Courtesy of Will Humphreys, University of Liverpool)
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9.74 (a) Right lateral and (b) DV thoracic radiographs of an 11-year-old neutered Yorkshire Terrier bitch with stage B2 MMVD and concurrent mild valvular aortic stenosis. The aortic arch is prominent on the DV view (arrowed) and was dilated during echocardiography. The dog also had hyperadrenocorticism and systemic hypertension, which may contribute to the changes in the cardiac silhouette.
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9.75 Newfoundland with subaortic stenosis. (a) Right parasternal long-axis four-chamber view and (b) short-axis view (diastolic frames). There is concentric left ventricular hypertrophy with hyperechoic papillary muscles and subendomyocardium. The increased echogenicity is consistent with myocardial ischaemia or fibrosis.
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9.76 The same Newfoundland as in Figure 9.75. (a) Right parasternal long-axis five-chamber view, which shows the aorta. There is a marked subvalvular muscular ridge from the basal septum, resulting in subvalvular aortic stenosis. The aortic valve leaflets look thick in this diastolic frame, but a systolic frame showed that they opened normally and the apparent increased valve thickness may be a secondary change in response to turbulent high-velocity flow. Post-stenotic dilatation of the ascending aorta is apparent. (b) Colour flow Doppler superimposed on a 2D image similar to (a). (bi) In systole, the turbulent flow can be seen to occur at the site of the subvalvular ridge. (bii) In diastole, aortic regurgitation can be seen. Ao = aorta. The same Newfoundland as in Figure 9.75. (c) This right parasternal five-chamber view shows a steep angle between the longitudinal line of the IVS and the line of the aorta. Reduced aortoseptal angle (*) has been implicated in postnatal (acquired) changes in the subvalvular region worsening or causing subvalvular obstruction. (d) Continuous wave Doppler from a subcostal view aligned with left ventricular outflow tract and aortic flow. Peak velocity is over 6 m/s, which corresponds to an LV–Ao pressure gradient exceeding 144 mmHg (severe stenosis). Ao = aorta.
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9.77 Right parasternal five-chamber view of a Maine Coon cat with valvular and supravalvular aortic stenosis. Two focal regions of narrowing are identified in the LVOT and there is dilatation of the post-stenotic aorta (Ao). (© J. Dukes-McEwan)
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9.78 German Shepherd Dog with subvalvular aortic stenosis. (a) Right parasternal five-chamber view. Note the prominent ridge in close proximity to and just below the aortic valve. The aortoseptal angle does not appear reduced in this dog. (b) Right parasternal five-chamber view, showing a colour Doppler map of the aortic outflow during systole. Note the turbulent flow within the aorta due to the stenosis. (c) Continuous wave Doppler trace from the aorta obtained from a subcostal position. A maximal aortic velocity of 3.99 m/s was recorded. Ao = aorta. (© J. Dukes-McEwan)
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9.79 The same Newfoundland as in Figures 9.75 and 9.76. These images were obtained 2 years later, when the dog was developing myocardial failure. (a) Note the more rounded, dilated LV. The LA was also dilated and mitral regurgitation had developed. The LV walls are no longer subjectively concentrically hypertrophied, and there are focal hyperechoic regions within the myocardium (possible fibrosis). (b) Subcostal continuous wave Doppler. Aortic velocity has reduced from over 6 m/s to less than 4 m/s, reflecting the myocardial dysfunction.
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9.80 Lateral angiocardiogram of a dog with subaortic stenosis. The contrast medium was injected in the RA and this is the levophase of the study, 7 seconds after injection of the contrast medium. There is clear narrowing of the subaortic region (arrowed) and mild post-stenotic dilatation of the aorta (Ao). Some degree of concentric hypertrophy of the LV can also be seen on this view. (Courtesy of J. Buchanan)
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9.81 Thoracic radiographs obtained from an 11-year-old Cocker Spaniel with an asymptomatic restrictive VSD. There is mild generalized cardiomegaly. (a) The DV view shows enlargement of the left caudal lobar pulmonary artery and vein. (b) The lateral view shows increased vascularity in the caudodorsal lung field. These findings are consistent with pulmonary overcirculation.
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9.82 French Bulldog puppy diagnosed with a restrictive VSD and a peritoneopericardial diaphragmatic hernia (not shown). (a) Right parasternal long-axis five-chamber view showing the turbulent colour flow jet crossing the perimembranous part of the IVS, just below the aortic valve leaflets, into the inflow part of the RV, just below the tricuspid valve leaflets. (b) Right parasternal short-axis view confirming the VSD flow is into the inflow part of the RV. (c) Spectral Doppler with continuous wave cursor placed parallel to flow, from the right parasternal five-chamber view. Velocity is high, at over 4.5 m/s, reflecting a normal expected pressure gradient between the LV and RV of over 81 mmHg. This is, therefore, a restrictive VSD. Ao = aorta.
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9.83 Right parasternal long-axis five-chamber view from an 8-month-old male British Shorthaired cat, with colour flow Doppler showing VSD flow crossing the perimembranous IVS into the RV. Although both ventricles appear volume overloaded, this cat was asymptomatic at the time. Ao = aorta.
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9.84 Boxer puppy diagnosed with a large VSD associated with left-sided volume overloading. (a) Right parasternal four-chamber view in diastole showing mild left atrial dilatation and a dilated, rounded LV. (b) Colour flow Doppler of a right parasternal five-chamber view in systole showing VSD flow crossing the IVS from beneath the aortic valves in the LV to the inflow part of the tricuspid valves. (c) Continuous wave Doppler of VSD flow. Peak velocity was over 4 m/s, suggesting a preserved LV–RV pressure gradient and lack of significant pulmonary hypertension. (d) Colour flow Doppler of a left parasternal cranial view optimizing alignment with the pulmonic trunk (PA). This shows colour variance and turbulent flow through the pulmonic valve (arrowed). (e) Continuous wave Doppler of pulmonary outflow. Peak velocity was 2.87 m/s, and there was no significant step-up between the RVOT and pulmonic trunk. This is called ‘relative pulmonic stenosis’ caused by increased volume of flow across normal pulmonic valves. The calculated flow across the pulmonic trunk compared with the aorta (Qp:Qs) was 3.26:1, confirming significant pulmonary overcirculation and resulting left-sided volume overload. Ao = aorta.
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9.85 Images from an 11-month-old male Border Collie with a VSD and pulmonary arterial hypertension (Eisenmenger’s syndrome) that presented with severe exercise intolerance and cyanosis. There was no echocardiographic evidence of any form of pulmonic stenosis. (a) Right parasternal four-chamber view, showing marked concentric hypertrophy of the RV leading to flattening of the IVS. (b) Right parasternal five-chamber view, showing the VSD in the basal IVS. This was 0.58 cm in diameter (callipers). (c) The VSD flow was bidirectional: (ci) In early systole (end of QRS complex) it was left-to-right. (cii) In late systole (end of T wave) it was right-to-left. (d) High pulse repetition pulsed wave Doppler confirming the bidirectional nature of the VSD flow: flow is left-to-right above the baseline and right-to-left below the baseline. The cursor is positioned parallel to VSD flow in the right parasternal five-chamber view. Ao = aorta.
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9.86 Lateral angiocardiogram of a 2-year-old German Shepherd Dog with a VSD. The contrast medium was injected in the LV and shunting can be seen from the LV to the RV through a membranous VSD (arrowed). There is also eccentric hypertrophy of the LV and apparent dilatation of the LA. (Courtesy of J. Buchanan)
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9.87 (a) DV and (b) lateral thoracic radiographs of a 2-year-old male German Shepherd Dog diagnosed with an ASD. There is mild cardiomegaly, which appears to be predominantly right sided, with increased sternal contact on the lateral view and a prominent right atrial region on the DV view. Pulmonary vasculature is within normal limits.
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9.88 (a) DV and (b) lateral thoracic radiographs of a 5-year-old Persian cat, diagnosed by echocardiography with a partial atrioventricular canal (endocardial cushion) defect with a septum primum ASD and mitral and tricuspid regurgitation. The cat had moderate pulmonary hypertension. There is a moderate diffuse unstructured parenchymal opacification of both lungs likely highlighted by obesity and poor lung inflation. The cardiac silhouette is enlarged with a VHS of roughly 10, without specific chamber enlargement. The pulmonary veins and arteries are moderately enlarged. The cat was reported to be asymptomatic; it was referred for assessment as its congenital heart murmur had become louder.
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9.89 Right parasternal four-chamber view of the same dog as in Figure 9.86. Dual image showing defect in mid-atrial septum in 2D (left) and superimposed colour flow Doppler (right) showing left-to-right flow. Location is consistent with an ostium secundum ASD. The right heart is prominent, consistent with volume overload associated with the left-to-right shunting.
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9.90 Right parasternal long-axis four-chamber view of a Boxer with a very high defect in the interatrial septum, resulting in left-to-right flow. This is consistent with a sinus venosus defect. (© J. Dukes-McEwan)
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9.91 Right parasternal long-axis four-chamber view of the same cat as in Figure 9.88. The atrioventricular valves are abnormal, both on the same plane, which is consistent with atrioventricular valve dysplasia. There is virtually no evidence of an interatrial septum (except very dorsally in the atrium). These findings are consistent with an ostium primum ASD and, together, the findings are consistent with an endocardial cushion defect. The right heart is dilated and shows concentric hypertrophy of the RVFW; the cat was confirmed to have mild pulmonary hypertension.
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9.92 7-month-old male Cocker Spaniel that was diagnosed with both a double-chambered RV and pulmonic stenosis with a hypoplastic pulmonic trunk. (a) Right parasternal four-chamber view. Note the severe concentric hypertrophy of the right ventricular free wall. The interatrial septum appears to have two components. (b) Colour flow Doppler shows flow between the interatrial septum components and across the interatrial septum, from right-to-left (blue) during diastole, as a consequence of the increased right heart pressures. These findings are consistent with a patent foramen ovale (PFO).
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9.93 (a) DV and (b) right lateral thoracic radiographs from a 2-year-old neutered female Toyger cat with dyspnoea and initial response to diuretic treatment that was subsequently diagnosed with mitral valve dysplasia and subaortic stenosis. The radiographs show left-sided cardiomegaly and a diffuse, patchy interstitial lung pattern consistent with pulmonary oedema.
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9.94 A 4-year-old male English Springer Spaniel diagnosed with mitral valve dysplasia and being treated for left-sided CHF. (a) Right parasternal four-chamber view. There is marked left atrial and left ventricular dilatation with eccentric hypertrophy. The mitral valve does not open fully, with a ‘hockey stick’ appearance to the anterior leaflets and a relatively immobile posterior leaflet. In addition, the mitral valve did not close to the level of the mitral annulus during systole, although this finding can be attributed to the altered geometry of the LV affecting the mitral valve apparatus. (bi) Left apical four-chamber view confirming mitral regurgitation on colour flow Doppler. (bii) Continuous wave Doppler of mitral regurgitation.
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9.95 A 2-year-old French Bulldog known to have a heart murmur but investigated only after developing left-sided CHF and subsequently diagnosed with mitral valve dysplasia with severe mitral regurgitation. (a) Right parasternal long-axis four-chamber view during ventricular systole. The mitral valve is abnormal, with a very long anterior leaflet and relatively immobile, short posterior leaflet. The anterior leaflet prolapses and overlaps the posterior leaflet. (b) Left apical four-chamber view with colour flow Doppler confirming an eccentric jet of mitral regurgitation coursing around the LA (coandal effect).
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9.96 (a) Right parasternal long-axis four-chamber view and (b) short-axis view at the papillary muscle level of a 3-month-old male Old English Sheepdog with mitral valve dysplasia and left-sided CHF. There was a single papillary muscle, which was large, with a well demarcated hyperechoic tip, attached to short chordae on both mitral valve leaflets. There is also a small pericardial effusion.
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9.97 A 4-year-old Welsh Terrier with evidence of left-sided cardiomegaly on CT, but no clinical signs referable to cardiac disease. No heart murmur was detected. (a) M-mode at mitral valve level showing abnormal mitral valve motion. The anterior leaflet (AMV) moves towards the IVS with restricted excursion and shows delayed partial closure during diastasis prior to atrial contraction (reduced EF slope). The most striking finding is that the posterior leaflet (PMV) does not move in the opposite direction towards the LVFW, but is tethered to the AMV, so its movement parallels that of the AMV. The valve is thick and the M-mode confirms incomplete opening. (b) Right parasternal four-chamber view during late diastole (associated with atrial contraction). The mitral valve leaflets did not open completely, appearing tethered and with a ‘hockey stick’ appearance. The colour flow Doppler shows colour variance of transmitral flow on the ventricular side of the mitral valve. (c) Left apical four-chamber view continuous wave Doppler of transmitral flow, showing increased E and A wave velocities, with the A wave higher than the E wave (E:A ratio <1) indicating dependence on atrial contraction to achieve ventricular filling. The E wave shows slow deceleration, so the A wave starts before the E wave is completed. These findings are all consistent with mitral stenosis. This case did not have mitral regurgitation.
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9.98 A 2-year-old male Border Terrier following a syncopal episode. (a) Right parasternal four-chamber view, showing marked concentric left ventricular hypertrophy but subjectively normal left atrial size. The anterior mitral valve leaflet appeared slightly thick and elongated, and during systole this was pushed into the left ventricular outflow tract. This resulted in dynamic left ventricular outflow tract obstruction and mild mitral regurgitation. (b) M-mode at the level of the mitral valve showing normal E and A peaks of the anterior leaflet during diastole, but also opening of the anterior leaflet during systole, confirming SAM (arrowed) of this anterior mitral valve leaflet. (c) Subcostal view with continuous wave Doppler confirming significant dynamic left ventricular outflow tract obstruction, with scimitar envelope, resulting from biphasic acceleration of left ventricular outflow. In a cat, these changes could be due to hypertrophic obstructive cardiomyopathy. In dogs, it is more common that they are associated with mitral valve dysplasia, especially with elongated anterior mitral valve leaflets. The SAM results in dynamic left ventricular outflow tract obstruction and the concentric left ventricular hypertrophy is likely secondary to this.
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9.99 (a) DV and (b) right lateral thoracic radiographs of a 10-month-old male Boxer with right-sided CHF. Ascites is confirmed by abdominal distension and poor abdominal serosal contrast. There is marked right ventricular and right atrial enlargement.
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9.100 A 4-month-old Labrador Retriever bitch with right-sided CHF (ascites) diagnosed with tricuspid dysplasia associated with severe tricuspid regurgitation, and mild aortic stenosis and pulmonic stenosis. (a) Right parasternal long-axis four-chamber view. There is severe right atrial and right ventricular dilatation. The mural tricuspid valve leaflet is directly attached to a papillary muscle and is tethered. The septal leaflet is very short and immobile. (b) The left apical four-chamber view confirms severe right atrial and right ventricular dilatation and abnormal tricuspid valve leaflets, which appear apically displaced. This systolic frame confirms poor coaptation between both tricuspid valve leaflets. (c) Colour flow Doppler of the left apical four-chamber view; systolic frame confirming tricuspid regurgitation. (d) Continuous wave Doppler of the tricuspid regurgitation jet. Peak velocity is increased (nearly 4 m/s) because of the concurrent mild pulmonic stenosis.
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9.101 (a) DV and (b) lateral thoracic radiographs of a 5-month-old male Airedale Terrier with stunted growth, severe exercise intolerance and cyanosis due to tetralogy of Fallot. There is no generalized cardiomegaly, but there is evidence of right ventricular enlargement resulting in slight apex tipping on the lateral view. The aortic arch is prominent on both the lateral and the DV view. The lungs appear hyperinflated and relatively hypovascular.
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9.102 Border Collie with tetralogy of Fallot. (a) Right parasternal long-axis five-chamber view. The aorta (Ao) is overriding or dextroposed and a high VSD is present. (b) Right parasternal short-axis view obtained at the level of the heart base and optimized for the RVOT. The pulmonic valve is stenotic and the valves are thickened and echogenic. The pulmonic trunk (MPA) is hypoplastic. (c) Right parasternal long-axis five-chamber view with colour Doppler. Blood is shunting from right-to-left across the VSD. (© J. Dukes-McEwan)
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9.103 Domestic Shorthaired cat with tetralogy of Fallot. (a) A high VSD is evident on the right parasternal short-axis view and the colour flow map documents the right-to-left flow. (b) Continuous wave Doppler shows the right-to-left flow across the septal defect. (© J. Dukes-McEwan)
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9.104 Lateral angiocardiogram of a dog with tetralogy of Fallot. The contrast medium was injected in the RV. There is narrowing of the pulmonic trunk (MPA) at the infundibular level (arrowed) and there is simultaneous opacification of the pulmonic trunk and the aorta (Ao), which means that there is a right-to-left shunt. (Courtesy of J. Buchanan)
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9.105 (a) DV and (b) right lateral thoracic radiographs of an 11-week-old male Golden Retriever with severe ascites, imperforate CTD, patent foramen ovale and double-chambered RV. The DV view shows right heart enlargement, especially the RA. Both views confirm ascites and the DV view shows distension of the CdVC.
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9.106 A 6-month-old Boxer bitch that presented with ascites. This left apical four-chamber view shows that the RA is in two compartments: a high pressure caudal compartment (RA(cd)) and a low pressure cranial compartment (RA(cr)) above the tricuspid valve.
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9.107 Lateral angiocardiogram of a 6-month-old Boxer bitch with ascites due to CTD (same dog as in Figure 9.106). Angiocardiography was performed during a fluoroscopic study prior to intervention (balloon dilation of the perforated CTD membrane) with a pigtail catheter in the CdVC (arrowed). The dog is also lying on an echotable to facilitate intraprocedural transthoracic echocardiography (edge of cut-out with staples seen to left of image). The caudal RA is very dilated, as is the CdVC, and some contrast shows retrograde flow into a dilated coronary sinus (arrowhead). In this frame, contrast cannot yet be seen in the cranial RA or RV.
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9.108 A Ragdoll cat diagnosed with CTS. Left apical four-chamber view showing a very dilated LA and subjectively distended pulmonary veins. There is a membrane proximal to the mitral valve, with high-velocity turbulent flow crossing it. The mitral valve (MV) leaflets are open normally during diastole. This lesion is just proximal to the mitral valve. The LAA cannot be assessed from this image; a dilated LAA suggests the cat is more likely to have supravalvular mitral stenosis (SVMS). However, CTS and SVMS are very similar in pathophysiology.
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9.109 Cat with an endocardial cushion defect and an unusual cor triatriatum. (a) Left apical four-chamber view. Large confluent atrial and ventral septal defects are evident. (b) Right parasternal long-axis view. The ASD can be seen and an additional thin dividing membrane is evident within the common atrium, creating an extra chamber (A*). This was considered to be CTS; however, the decision as to whether the lesion is left- or right-sided is difficult when a common atrium is present. (© J. Dukes-McEwan)
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9.110 Lateral angiocardiogram in a cat with CTS. The contrast medium was injected in the RV after catheterization of the jugular vein. A levophase image is presented, where the contrast medium has reached the LA. The LA is enlarged and a linear filling defect is visible in its lumen, corresponding to the dividing membrane (arrowed). (Courtesy of J. Buchanan)
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9.111 (a) Left lateral and (b) DV thoracic radiographs of a 2-month-old intact crossbreed bitch with regurgitation and thin body condition due to a vascular ring anomaly. The oesophagus is severely segmentally enlarged (orange) cranial to the heart base, causing ventral tracheal deviation (yellow). The most common type of vascular ring anomaly is a PRAA with a persistent left ligamentum arteriosum. Based on the focal tracheal deviation to the left (arrowed), this dog has a PRAA. The ligamentum arteriosum cannot be seen with this type of study.
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9.112 Lateral oesophagram of a dog with a vascular ring anomaly associated with a PRAA, after oral administration of barium sulphate. There is accumulation of the contrast medium in a distended oesophagus cranial to the heart base and abrupt tapering at the level of the heart base. (Courtesy of J. Buchanan)
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9.113 Thoracic CT angiograms of a 14-week-old neutered crossbreed bitch with regurgitation and thin body condition. (a) Craniodorsal aspect, 3D volume rendered image. (b) Transverse CT image (arterial phase; soft tissue window) acquired at the level of the fourth thoracic vertebra (T4). Thoracic radiography performed by the referring veterinary surgeon showed segmental oesophageal enlargement cranial to the heart base. The clinical signs and segmental oesophageal enlargement were attributed to a congenital developmental vascular ring anomaly (*) formed by left and right aortic arches (double aortic arches). The ring encircles the trachea and oesophagus, the latter of which is enlarged cranial to the ring. Surgery was performed to ligate and transect the right aortic arch. The dog recovered well and was discharged. 1 = right aortic arch; 2 = left aortic arch; 3 = right subclavian artery; 4 = right common carotid artery; 5 = left common carotid artery; 6 = left subclavian artery; 7 = descending aorta; O = oesophagus; T = trachea.
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9.114 Lateral aortogram of a dog with aortic coarctation. Contrast medium was injected in the aortic arch after catheterization of the femoral artery. There is narrowing of the aorta caudal to the origin of the left subclavian artery, followed by marked dilatation of the aorta caudal to the stenosis. The catheter is seen curving around in the dilated portion of the aorta. (Courtesy of M. Herrtage)
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9.115 A 1-year-old spaniel with Marfan-like syndrome. (a) Multiplanar reconstruction of a CT angiogram (sagittal image). There is severe dilatation of the aortic root. This affects the entire aortic arch, including the brachiocephalic and left subclavian arteries. Aortic regurgitation can also be noted. The descending aorta is within normal limits. (bi) Right parasternal long-axis five-chamber view showing the aortic valves and ascending aorta during systole. (bii) Colour flow Doppler from a left apical five-chamber view showing the aorta (Ao) and aortic regurgitation during diastole.
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9.116 A 4-year-old Great Dane bitch that was being screened for dilated cardiomyopathy, with no clinically significant cardiac disease apparent at time of examination. A dilated coronary sinus was noted as an incidental finding. This is usually associated with a PLCrVC. (a) Right parasternal long-axis view showing the dilated coronary sinus, which courses around the left atrioventricular groove, opening into the RA (arrowed). (b) Left apical four-chamber view optimized for the dilated coronary sinus (arrowed), which can be seen opening into the RA. A 4-year-old Great Dane bitch that was being screened for dilated cardiomyopathy, with no clinically significant cardiac disease apparent at time of examination. A dilated coronary sinus was noted as an incidental finding. This is usually associated with a PLCrVC. (c) With a standard right parasternal long-axis four-chamber view, the dilated coronary sinus is often seen in short axis in the left atrioventricular groove (arrowed).
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9.117 (a) Transverse, (b) sagittal and (c) dorsal multiplanar reformatted contrast-enhanced CT images (soft tissue reconstruction) of a PLCrVC (arrowed) in a dog. (Courtesy of Will Humphreys, University of Liverpool)
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9.118 (a) Right lateral and (b) DV thoracic radiographs from a Cocker Spaniel with coughing and dyspnoea. There is generalized cardiomegaly with left atrial enlargement and pulmonary venous distension. There is a caudodorsal mixed interstitial–alveolar lung pattern, consistent with pulmonary oedema. Echocardiography confirmed that this dog had DCM resulting in the left-sided CHF.
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9.119 (a) Right lateral and (b) DV thoracic radiographs of a Dobermann with a history of several weeks coughing, recent syncopal episodes and then dyspnoea. DCM in the Dobermann is not associated with radiographic evidence of massive cardiomegaly, but there is left atrial and left ventricular enlargement. Note the pulmonary venous distension (arrowed) and the predominantly perihilar mixed interstitial and alveolar infiltrate.
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9.120 A Hungarian Vizsla with DCM and left-sided CHF. (a) Right parasternal long-axis four-chamber view in (ai) diastole and (aii) systole. There is very little difference in left ventricular area between diastole and systole because of severely impaired left ventricular systolic function. The LV is subjectively dilated and rounded, with relatively thin walls. The dog also has an arrhythmia. (bi) Left ventricular M-mode with the cursor positioned on the short-axis view, at the level of the chordae tendinae, bisecting the LV. There is markedly impaired LV systolic function. (bii) Mitral M-mode with the cursor positioned on the short-axis ‘fish-mouth’ view, showing the increased E point to septal separation. (c) Colour flow Doppler using a right parasternal long-axis four-chamber view showing mitral regurgitation, likely to be a consequence of stretch of the mitral annulus with the left ventricular and left atrial dilatation.
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9.121 A Cocker Spaniel with DCM. Echocardiographic measurement of left ventricular volumes in (a) diastole and (b) systole by Simpson’s method of discs. The EDV is 80 ml and the ESV is 55 ml. The calculated left ventricular ejection fraction was low at 31.2% and the left ventricular ESVI was increased at 90 ml/m. The sphericity index was also calculated from the diastolic left ventricular length and M-mode diastolic diameter: this was reduced at 1.4, confirming a rounded LV.
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9.122 A Boxer with ARVC, collapse and ventricular tachycardia. The arrhythmia was treated. (a) The right parasternal long-axis and (b) short-axis views show dilatation of the RA and RV. (c) The apical sternal right parasternal view shows dysplastic papillary muscles in the RV apex. Ao = aorta.
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9.123 (a–f) A 2-year-old Border Terrier with frequent syncopal episodes when excited and a heart murmur due to HOCM. There is marked concentric hypertrophy of the LV, evident from (a) the right parasternal long-axis four-chamber view, (b) the five-chamber view and (c) the short-axis view. (b) The aortic valves, LVOT and ascending aorta are grossly normal. However, the mitral valve anterior leaflet is moving towards the basal septum (*) in this early systolic frame (endocardial thickening of the basal septum may be consistent with a ‘kissing’ lesion). (d) The presence of SAM of the anterior mitral valve leaflet (arrowed) is confirmed by the superior temporal resolution of M-mode at mitral valve level. SAM results in dynamic LVOT obstruction. (e) This can be documented from a left apical view. There is increased aortic outflow velocity with a biphasic acceleration slope (*). In this example, continuous wave Doppler shows aortic peak velocities to be >6 m/s. (f) SAM also results in mitral valve incompetence and colour flow Doppler typically shows an eccentric mitral regurgitation jet, coursing towards the posterior-lateral wall of the LA. (g–h) Transverse CT images of a 9-year-old Dalmatian with a cough. There is marked thickening of the left ventricular myocardium and reduced lumen, and dilatation of the left atrium as well as perivascular pulmonary oedema. HOCM with right and left congestive heart failure was confirmed using echocardiography. Ao = aorta.
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9.124 (a) Right lateral and (b) DV thoracic radiographs of a cat with apparently sudden onset left-sided CHF. There is marked left atrial enlargement and dilatation of the LAA, which results in the appearance of a ‘valentine heart’ on the DV view. The pulmonary arteries and veins are dilated (pulmonary hypertension may be secondary to left-sided heart failure in the cat). The pulmonary opacification associated with cardiogenic pulmonary oedema in the cat can be patchy and variable in distribution, as indicated here. This cat also has pericardial fat.
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9.126 A young neutered male Domestic Shorthaired cat with HOCM. (a) Right parasternal long-axis four-chambered view in diastole showing concentric hypertrophy of the left ventricular wall (symmetrical in this case). (b) Right parasternal short-axis view confirming the severe left ventricular hypertrophy. In systole, there is obliteration of the left ventricular cavity. The right ventricular wall is also subjectively hypertrophied. (c) Right parasternal long-axis five-chamber view during systole. The anterior mitral valve leaflet moves towards the IVS during systole – this is SAM. This narrows the left ventricular outflow tract, causing dynamic obstruction to ejection, and also results in mitral regurgitation. (d) Colour flow Doppler superimposed on similar image to (c). This shows the ‘double jet’ typical of HOCM, with left ventricular outflow tract obstruction causing colour variance, and there is an eccentric jet of mitral regurgitation. Ao = aorta. A young neutered male Domestic Shorthaired cat with HOCM. (e) Left ventricular M-mode with the cursor positioned from a short-axis view, bisecting the left ventricular cavity. With HCM, the M-mode typically has a cluttered appearance and it can be difficult to avoid the hypertrophied papillary muscles. (f) M-mode at the level of the mitral valve (cursor positioned from the short-axis ‘fish-mouth’ 2D view). The mitral valve anterior leaflet opens normally in diastole but demonstrates SAM. (g) M-mode at the level of the aortic valves. The M-mode cursor was positioned on a right parasternal short-axis view of the heart base. The aortic valves partially close prematurely (arrowed). This is a consequence of SAM, which obstructs left ventricular outflow during systole. (h) Right parasternal short-axis view at the level of the aortic valve, optimizing the left atrial size. The LA is dilated, although the LAA appears dilated to a greater extent than the body of the LA. Ao = aorta.
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9.127 Right parasternal long-axis four-chamber view from a cat with HCM and normal left atrial diameter (14.4 mm) during ventricular systole; <16 mm is normal.
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9.128 Right parasternal long-axis four-chamber view obtained at the end of ventricular systole (frame before the mitral valve opens) showing left atrial dilatation in a cat with HCM. The atrial septum is pushed to the right, and the atrium has a rounded appearance. The maximal diameter exceeds 16 mm, which confirms left atrial enlargement.
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9.129 Continuous wave Doppler from a left apical five-chamber view of a cat with asymptomatic HOCM. The cursor is aligned with the colour variance in the left ventricular outflow tract, with dynamic left ventricular outflow tract obstruction due to SAM of the anterior mitral valve. The biphasic acceleration of the left ventricular outflow tract and aortic envelopes can be seen, with peak velocity just less than 4 m/s.
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9.130 Aortic M-mode from an asymptomatic cat with HOCM, showing the mid-systolic closure and biphasic opening of the aortic valves during ejection typical of dynamic left ventricular outflow tract obstruction, producing a double-diamond appearance (superimposed in blue).
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9.132 Mitral inflow patterns. (a) Normal mitral inflow with E wave velocity of <2 but >1 x A wave velocity. (b) Abnormal relaxation with A wave velocity >E wave velocity. As active relaxation (lusitropy) of the LV is compromised, E wave velocity is reduced and E wave deceleration time is prolonged. IVRT is prolonged. Atrial contraction is important to achieve ventricular filling. (c) With development of the disease, left atrial pressures increase and E wave velocity increases, giving a relatively normal E:A ratio again (pseudonormalization). (d) Further worsening of the disease, with high left atrial pressure and a stiff, poorly compliant LV, can result in a high E wave velocity, short E wave deceleration time and E:A velocity ratio of >2 (restrictive filling pattern).
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9.133 Pulsed wave Doppler echocardiograms showing mitral inflow patterns from cats with myocardial disease. (ai) A cat with HOCM that was presented for investigation of an asymptomatic heart murmur. Note the abnormal relaxation pattern (E<A; prolonged E deceleration time). (aii) Re-evaluation 6 months later. The cat was still asymptomatic but there is evidence of increased left atrial pressure; the E wave velocity is increased, although there is still E:A reversal and evidence of abnormal relaxation. (b) A cat with pseudonormalization. Note that although the left atrial pressures have increased, the abnormal relaxation is now masked, and other methods are required to document the diastolic dysfunction. (c) A cat with severe biventricular failure and RCM. A restrictive filling pattern with probable left atrial dysfunction is shown, with E much greater than A, low-velocity A wave and short E wave deceleration time.
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9.134 Measurement of IVRT in cats with myocardial disease using pulsed wave Doppler echocardiography. (a) Normal cat, with time measurement from aortic valve closure to onset of mitral flow. (b) A cat with abnormal relaxation time, showing increased IVRT (>65 ms). (c) A cat with a restrictive filling time, showing very short IVRT (<55 ms).
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9.135 Assessment of PVF pattern in cats with myocardial disease using pulsed wave Doppler echocardiography. (a) Normal, middle-aged cat with D>S. (b) A cat with abnormal relaxation, with increased S wave (measurement 2) and lower D wave (measurement 3) velocity but increased velocity of the atrial reversal wave (Ar) (measurement 1). (c) A cat with a restrictive filling pattern, with normal atrial function (increased Ar). D wave velocity exceeds S, and D deceleration is rapid.
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9.136 A cat with RCM. Marked left atrial enlargement is apparent on both (a) the right parasternal long-axis four-chamber view (33 mm diameter) and (b) the right parasternal short-axis view at the level of the aortic valves. (b) On the short-axis view, there is a poorly defined thrombus (arrowed) in the LAA with a real-time image showing spontaneous echocontrast in the LA. This cat had atrial fibrillation with occasional ventricular premature complexes. (c) A modified left parasternal cranial view, optimized for the LAA. The thrombus in the LAA can be seen with spontaneous echocontrast appearing as ‘smoke’, swirling in the junction of the LAA and LA. (d) right parasternal four-chamber view of the LV showing an irregular endocardium, particularly on the septum, and a probable adhesion crossing the LV chamber. Ao = aorta; MV = mitral valve.
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9.137 Cranial left parasternal view optimized for the LA and LAA in a Siamese cat with the endomyocardial form of restricted cardiomyopathy, with an organized thrombus (arrowed) within the LAA. PA = pulmonic trunk.
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9.138 A cat with the endomyocardial form of RCM. (a) Left apical four-chamber view, showing a bridging scar crossing the LV (arrowed). A cat with the endomyocardial form of RCM. (b) Colour flow Doppler shows that the bridging scar is associated with turbulence in the mid-LV in both (bi) diastole and (bii) systole.
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9.139 (a) Right lateral and (b) DV thoracic radiographs of a cat with DCM. There is a large-volume bilateral pleural effusion, masking detail of the cardiac silhouette and the lung fields. From the degree of tracheal elevation, the cardiac silhouette appears to have marked generalized enlargement.
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9.140 M-mode echocardiogram of a cat with DCM, showing a pleural effusion and marked hypokinesis, especially of the LVFW.
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9.141 An elderly cat with untreated, probably long-standing, hyperthyroidism. (a) The right parasternal long-axis four-chamber view shows four-chamber dilatation. (b) In real time, the LV was hypokinetic, which is indicated on the M-mode view. Notice that the LVFW is not functioning on the M-mode, and the wall is thin. A segmental region of the thin posterior wall is shown in (a) (*). This may correspond to a myocardial infarct (although post-mortem confirmation was not achieved in this cat).
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9.142 A cat later confirmed to have ARVC. (a) Right lateral thoracic radiograph. There is right-sided heart enlargement, and ascites with a dilated CdVC supports right-sided CHF. (b) Right parasternal long-axis four-chamber view, indicating marked right atrial and right ventricular enlargement.
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9.143 A cat with ARVC. (a) Right parasternal long-axis four-chamber view. Colour flow mapping indicates the presence of tricuspid and mitral regurgitation due to stretch of the atrioventricular annuli secondary to myocardial disease, although the RV is predominantly affected. (b) M-mode, showing dilatation of both ventricles and impaired left ventricular systolic function. This cat was in atrial fibrillation.
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9.144 End-stage (non-specific) cardiomyopathy in a cat with biventricular CHF. Echocardiography follows thoracocentesis. (a) Right parasternal four-chamber view, showing residual pleural effusion (Pl eff), a trivial pericardial effusion (PE) and four-chamber dilatation. (b) Left ventricular M-mode indicating severely impaired left ventricular systolic function.
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9.145 A whippet with steroid responsive meningoarteritis. Right parasternal four-chamber view, showing a small pericardial effusion and spontaneous echocontrast in the LV (arrowed). These changes are associated with an inflammatory state. Left ventricular systolic function was also impaired (not shown). PE = pericardial effusion.
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9.146 A Cocker Spaniel with myxomatous degenerative valvular disease with high-velocity mitral regurgitation, associated with systemic hypertension, which caused concentric left ventricular hypertrophy (aortic stenosis was excluded). (a) Right parasternal long-axis four-chamber view and (b) short-axis view at the level of the papillary muscles, showing mild left atrial dilatation and concentric hypertrophy of the LV.
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9.147 Thoracic radiographs of a 2-year-old neutered male mixed-breed dog subsequently diagnosed with angiostrongylosis and severe pulmonary arterial hypertension. All views show pulmonary opacification, which is predominantly peripheral, typical of angiostrongylosis. The (a) right and (b) left lateral views show increased sternal contact of the cardiac silhouette with apex tipping, consistent with right ventricular hypertrophy. Thoracic radiographs of a 2-year-old neutered male mixed-breed dog subsequently diagnosed with angiostrongylosis and severe pulmonary arterial hypertension. All views show pulmonary opacification, which is predominantly peripheral, typical of angiostrongylosis. (c) The DV view shows a pulmonary knuckle (arrowed) and distended caudal lobar pulmonary arteries (*).
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9.148 (a) Right lateral and (b) DV thoracic radiographs of a dog with (heartworm) infection. The pulmonary arteries are moderately dilated and tortuous (arrowed). (Courtesy of M. Sullivan)
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9.149 (a–e) A 10-year-old Jack Russell Terrier with severe pulmonary arterial hypertension associated with a form of interstitial lung disease (cause not identified). (a) Right parasternal long-axis four-chamber view, showing right heart dilatation, with hypertrophy of the RVFW and flattening of the IVS. The right pulmonary artery (RPA) dorsal to the LA is very dilated. (b) Short-axis view at ventricular level, confirming flattening of the IVS and underfilling of the LV due to pressure overload of the RV. (c) Right parasternal short-axis view, optimizing the pulmonic trunk (PA), which is very dilated compared with the aorta (Ao). The RPA is also very dilated. (d) Tricuspid regurgitation (optimized alignment from a right parasternal short-axis view). Peak velocity (TR Vmax) was 5.7 m/s (reference value <2.7 m/s) corresponding to an RV–RA pressure gradient (TR maxPG) of 130 mmHg (reference value <30 mmHg). In the absence of pulmonic stenosis, this reflects severe systolic pulmonary arterial hypertension. (e) A 10-year-old Jack Russell Terrier with severe pulmonary arterial hypertension associated with a form of interstitial lung disease (cause not identified). Continuous wave Doppler, from the right parasternal short-axis view, optimizing with the pulmonic regurgitation jet seen on colour Doppler. Peak velocity (PR Vmax) was 4.03 m/s (reference value <2.2 m/s) corresponding to a diastolic PA–RV pressure gradient (PR maxPG) of 65 mmHg (reference value <20 mmHg). This is severe diastolic pulmonary arterial hypertension. (f) Pulmonary flow (pulsed wave spectral Doppler) from a dog with pulmonary hypertension due to angiostrongylosis (same dog as in Figure 9.147). This shows steep acceleration and delayed deceleration with mid-systolic notching in the pulmonary envelopes. However, this must be interpreted with caution since it can be artefactual if there is suboptimal alignment with pulmonary flow.
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9.150 (a) Right parasternal long-axis four-chamber view and (b) short-axis view from a crossbreed dog. The myocardium appears thickened with a heterogeneous patchy increased echogenicity. There is a small amount of pericardial effusion. This was sampled and cytology confirmed the diagnosis of cardiac lymphoma. (c) After 9 days of staged chemotherapy, the walls had reduced thickness.
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9.151 An 11-year-old male Golden Retriever with collapse, anaemia and paroxysmal ventricular tachycardia. (a) The right parasternal long-axis four-chamber view, (b) short-axis view and (c) left apical four-chamber view all show evidence of thickened myocardial walls, with disrupted architecture and numerous hypoechoic lesions of various sizes. (d) Post-mortem examination showed the entire myocardium was affected by a disseminated haemangiosarcoma. (Courtesy of R. Irvine)
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9.152 Staging of MMVD based on the ACVIM consensus guidelines for the diagnosis and treatment of MMVD in dogs ( ). Ao = aorta; LVIDdN = left ventricular internal diameter in diastole normalized for bodyweight by allometric scaling; MR = mitral regurgitation.
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9.153 Radiographic progression of volume overload associated with MMVD in a Cavalier King Charles Spaniel. (ai, bi, ci) Right lateral and (aii, bii, cii) DV views. (a) Initial radiographs (at 7 years and 1 month of age) to investigate an increase in grade of heart murmur, which had been first detected at least 18 months prior to imaging. Mild left-sided cardiomegaly is evident on the lateral view (VHS 11.75 v). Echocardiography did not fully meet stage B2 criteria at this time. (b) Radiographs repeated 9 months later. The cardiomegaly has progressed (VHS 12.25 v). The DV view shows an increase in left atrial size, with greater lateral deviation of the left caudal lobar bronchus. Echocardiography was consistent with advanced stage B2 MMVD. Treatment with furosemide was initiated 3 months later after an increase in resting respiratory rate. (c) Radiographs repeated 16 months after initial radiographs, to further investigate a problematic persistent cough. The cardiomegaly has continued to progress (VHS 13 v). There has been a further increase in left atrial and left ventricular enlargement. The pulmonary veins are mildly congested and there is a perihilar unstructured interstitial pattern which is attributed to the enlarged left atrium and may be cardiogenic pulmonary oedema. These radiographs were obtained under anaesthesia prior to tracheobronchoscopy, which revealed bronchial collapse associated with bronchomalacia and mild tracheal collapse.
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9.154 A Whippet with advanced, stage B2 MMVD. (a) The nodular thickening of the anterior leaflet tip can be seen (diastolic frame). (b) In systole, there is severe prolapse of the anterior leaflet giving the impression of a parachute valve (systolic frame). (c) This is associated with severe mitral regurgitation with an eccentric jet (systolic frame).
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9.155 Systolic frame from a right parasternal long-axis four-chamber view of a Cavalier King Charles Spaniel with Stage B1 MMVD, showing mitral valve prolapse. A line is drawn along the mitral annulus. In the Danish system of screening for mitral prolapse (shown here), lines are drawn perpendicular to the annulus line to the atrial side of the valve at three sites: the anterior (cranial or septal) leaflet, the coaptation point and the posterior (caudal or mural) leaflet, and the values in millimetres are summed. In the new UK scheme, the maximum prolapse distance is measured, rather than all three distances (which can sometimes be difficult to optimize on a single systolic frame).
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9.156 (ai, bi) Right parasternal short-axis and (aii, bii) M-mode echocardiograms of two dogs. Stage B2 criteria require both the LA:Ao and LVIDdN to be increased (≥1.6 and >1.7, respectively). Therefore, there can be a range in severity for stage B2, from (a) very mild (LA:Ao 1.61; LVIDdN 1.72) to (b) advanced (LA:Ao 2.61; LVIDdN 2.18). Both these dogs would meet inclusion criteria for the EPIC study and may, therefore, benefit from being prescribed pimobendan.
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9.157 (a) Normal LA with a square appearance during systole in a dog with MMVD stage B1. (b) Stage C decompensated MMVD, with bowing of the interatrial septum and rounded appearance to the LA, consistent with increased left atrial pressure. (ai, bi) Right parasternal long-axis four-chamber views, showing measurement of left atrial diameter at the end of systole (LA max). (aii, bii) Right parasternal long-axis five-chamber views showing the aortic annulus. The aortic annulus diameter is measured on a systolic frame, between open aortic valve leaflets. The ratio (LA max:Ao annulus) is calculated; normal values are <2.5.
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9.158 Use of colour flow Doppler to estimate severity of mitral regurgitation. Left apical four-chamber views with colour interrogation of the mitral valve, during ventricular systole, from a Cavalier King Charles Spaniel with end-stage biventricular CHF. (a) Colour flow showing the mitral regurgitation jet area almost filling the LA. However, it should be noted that jet area is not recommended to assess severity of mitral regurgitation as it is influenced by a range of other factors. (b) Magnified image. The flow convergence leading to a semicircle of colour aliasing on the ventricular side of the mitral valve, prior to the regurgitant orifice, is consistent with severe mitral regurgitation if the Nyquist limit is high. With a central jet of mitral regurgitation, the proximal isovelocity surface area (PISA) can determine the mitral regurgitant volume, but this is not applicable with eccentric or multiple jets, common in MMVD. (c) Magnified image. The width of the vena contracta (width of jet as it becomes turbulent through the mitral regurgitant orifice) correlates with severity of mitral regurgitation. It can be indexed to aortic annulus diameter.
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9.159 Continuous wave spectral Doppler echocardiograms showing mitral regurgitation. (a) Cocker Spaniel with stage B2 MMVD. Typical mitral regurgitation spectral Doppler envelopes are tongue shaped, but the full spectral Doppler is not always evident unless mitral regurgitation is severe. The third spectrum is complete and could be used to measure mitral regurgitation velocity (normally 5–6 m/s). (b) Cavalier King Charles Spaniel with stage D MMVD and biventricular CHF. The mitral regurgitation continuous wave spectral Doppler envelopes are more pointed with high left-sided filling pressures.
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9.160 Development of right-sided CHF due to pulmonary hypertension in a Cavalier King Charles Spaniel with advanced (stage D) MMVD. (ai) Right lateral and (aii) DV thoracic radiographs showing ascites, consistent with right-sided CHF. There is generalized cardiomegaly, with left atrial and left ventricular enlargement, resulting in apex shifting to the right. The lateral view with increased sternal contact suggests concurrent right ventricular enlargement. The DV view shows pulmonary venous congestion; the lobar pulmonary arteries are also increased in size. (b) Right parasternal long-axis four-chamber view showing marked right heart enlargement with flattening of the IVS, consistent with right ventricular pressure overload (pulmonary hypertension). There is a dilated coronary sinus (CS), initially thought to be due to a PLCrVC, but this reduced to normal size after treatment of the CHF and pulmonary hypertension. (ci) Left apical four-chamber view from the time of presentation, showing severe tricuspid regurgitation at increased velocity. (cii) Tricuspid regurgitation velocity was approximately 4 m/s (pulmonic stenosis was excluded). Therefore, from the modified Bernoulli equation, the RV–RA pressure gradient was calculated to be approximately 64 mmHg. The right atrial pressure was increased, as evidenced by the right-sided CHF signs, so pulmonary arterial systolic pressure was over 64 mmHg.
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9.161 Right parasternal long-axis four-chamber view from a dog with MMVD and rupture of a chorda tendina; this slender cord can be seen flicking into the LA during ventricular systole (arrowed).
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9.162 Right parasternal long-axis four-chamber view showing flail of the tip of the anterior mitral valve leaflet in early systole (arrowed), reflecting rupture of a major chorda tendina.
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9.163 Right parasternal long-axis four-chamber view from a small crossbreed dog receiving treatment for advanced MMVD with CHF. The dog had suddenly collapsed and was found to have a pericardial effusion with cardiac tamponade (diastolic collapse of the right atrial wall; arrowed). In a dog with a very dilated LA and cardiac tamponade, the possibility of a left atrial tear and pericardial haemorrhage must be considered.
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9.164 Right parasternal four-chamber views from a Labrador Retriever with right thoracic limb lameness, fever and subsequent development of neurological signs and a new heart murmur detected during hospitalization. (a) A vegetation can be seen on the ventricular side of the posterior mitral valve leaflet in diastole, which (b) flicked into the LA during systole. A smaller vegetation can be seen on the anterior leaflet during systole.
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9.165 Right parasternal long-axis five-chamber view of a Boxer with aortic valve vegetative endocarditis. A large, hyperechoic lesion can be seen on the ventricular side of the aortic valve in this diastolic frame (arrowed). Ao = aorta.
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9.166 Right parasternal long-axis four-chamber view showing pericardial effusion (arrowheads) as an anechoic region surrounding the heart. The right atrial wall shows some collapse (arrowed); this is cardiac tamponade and it indicates that pericardial pressure exceeds right atrial pressure.
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9.167 (ai) Lateral and (aii) DV thoracic radiographs of a 5-year-old cat with HCM and biventricular CHF. Unusually, this was associated with a large, recurrent pericardial effusion contributing to global generalized enlargement of the cardiac silhouette, without radiographic evidence of specific chamber enlargement. (b) Right parasternal four-chamber view of the same cat as in (a), showing a large pericardial effusion (arrowed). Asymmetrical hypertrophy of the LVFW can be seen, with left atrial dilatation. 72 ml of serosanguinous effusion was drained. (c) Lateral thoracic radiograph of an 11-year-old cat with a moderate pericardial effusion; the cardiac silhouette is ovoid and resembles a normal canine cardiac silhouette.
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9.168 Right parasternal short-axis view showing right ventricular inflow and outflow from a Border Terrier presenting with cranial caval syndrome. There is a heterogeneous mass in the region of the tricuspid valve, located mainly in the RA. There is a small pericardial effusion (PE) and an extensive extracardiac mass, only part of which is seen, outside the RVOT. This was an extensive haemangiosarcoma. Ao = aorta; CVC = caudal vena cava; PA = pulmonic trunk.
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9.169 Right parasternal four-chamber view showing a heterogeneous mass (arrowed) affecting the right atrioventricular groove of a 12-year-old Dachshund. Pericardial effusion (PE) had been drained one day previously, but residual effusion is evident. The myocardium of the RVFW also appears abnormal (*) suggesting infiltration. A presumptive diagnosis of haemangiosarcoma was made.
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9.170 (a) Right parasternal short-axis view at the level of the aortic valves and (b) left apical three-chamber view of a Staffordshire Bull Terrier with ventricular tachycardia. There was no pericardial effusion, but a periaortic heart base mass (possible chemodectoma) is shown. Ao = aorta.
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9.171 Right parasternal long-axis five-chamber view, optimizing an isoechoic, homogeneous mass within the LAA (arrowed) of a 10-year-old neutered Cavalier King Charles Spaniel bitch with preclinical MMVD. The appearance is most consistent with a myxoma, but this was not confirmed. LAA masses are rare. Ao = aorta.
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9.172 (a) Transverse, (b) dorsal and (c) sagittal multiplanar reformatted contrast-enhanced thoracic CT images (soft tissue reconstruction) of a large, rounded, heterogeneous soft tissue attenuating, mildly rim enhancing mass (probable haemangiosarcoma) arising from the region of the RA/atrioventricular groove (arrowed) in a dog. Multiple small soft tissue attenuating nodules are also visible within the lungs (disseminated metastasis). (Courtesy of Will Humphreys, University of Liverpool)
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9.173 (a) Sagittal, (b) dorsal and (c) transverse multiplanar reformatted contrast-enhanced CT thoracic images (soft tissue reconstruction) showing a large globoid, sharply marginated but heterogeneously contrast enhancing mass at the heart base (arrowed) displacing the caudal trachea to the right (possible chemodectoma). (Courtesy of Will Humphreys, University of Liverpool)
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9.174 Caudal right parasternal long-axis four-chamber view from a 1-year-old male German Shepherd Dog with a pericardial effusion (PE) resulting in cardiac tamponade and right-sided CHF. There is a hyperechoic ‘mass’ in the PE (arrowed), attached not to the heart but to the parietal pericardial wall. This was subsequently confirmed to be herniated fat associated with a very small PPDH.
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9.175 Continuous wave spectral Doppler showing respiratory variation in transmitral flow velocities in a dog with constrictive–effusive pericardial disease. (Courtesy of Urszula Bartoszuk)
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9.176 (ai) Right lateral, (aii) DV and (aiii) left lateral thoracic radiographs from a 4-month-old male Border Terrier with a PPDH including herniated liver in the pericardial sac. The dog also had a sternal cleft and large abdominal hernia. Generalized enlargement of the cardiac silhouette is seen, with a poorly defined diaphragmatic line. (b) Modified left apical five-chamber view from the same dog, showing the liver (arrowed) adjacent to the left ventricular wall. Ao = aorta.
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9.177 Pericardial cyst resulting in compression of the right heart in a 4-year-old crossbreed dog that had episodic collapse on severe exertion and, more recently, signs of right-sided CHF. The cyst is relatively thick-walled and filled with haemorrhagic contents. (Reproduced from with permission)
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9.178 Images from an 11-year-old neutered male Cocker Spaniel that had suffered an episode of collapse on exertion, without loss of consciousness but with apparent pain (yelping). The dog had stage B1 MMVD. The LAA was very dilated, suspected to be herniated through a pericardial defect. (ai) Right parasternal long-axis four-chamber view optimized for the dilated LAA. (aii) Left apical two-chamber view, showing the dilated LAA (arrowed) adjacent to the left ventricular wall. This was associated with apparent turbulence suggesting some mild obstruction associated with atrial systole (colour flow Doppler). (bi) DV and (bii) right lateral thoracic radiographs from the same dog, showing LAA enlargement on the DV view. (c) Transverse thoracic CT image with intravascular contrast material confirming the enlargement of the LAA. The pericardium could not be directly imaged to confirm LAA herniation outside the pericardium.
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9.179 Canine heart with herniation and incarceration of the RV through a large pericardial defect. (Courtesy of J. Buchanan)
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9.180 (a) Lateral and (b) VD thoracic radiographs of a 12-year-old male Golden Retriever with heartworm disease. The pulmonary arteries are extremely enlarged and tortuous (arrowed). The cardiac silhouette is rounded and right-sided cardiomegaly is present. Incidental tiny metallic opacities represent lead shot from a previous injury. (c) DV thoracic radiograph of a 4-year-old Staffordshire Bull Terrier with heartworm disease. This radiograph was acquired 3 months after treatment for caval syndrome and heartworm disease. Severe right-sided cardiac enlargement and pulmonic trunk enlargement (arrowed) are still evident.
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9.181 Selective lateral angiogram in a dog with chronic heartworm disease. Several catheters are present but angiography was performed via a catheter in the pulmonic trunk. The contrast medium fills a markedly dilated pulmonic trunk and its branches. The caudal lobar pulmonary arteries are also tortuous and truncated.
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9.182 VD thoracic radiograph of a 7-year-old cat with heartworm disease, showing moderate to severe enlargement and lack of tapering of the caudal lobar pulmonary arteries (arrowed).
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9.183 (a) Right parasternal short-axis view of the heart base and pulmonary arteries of a 7-year-old neutered male mixed-breed dog. Several adult worms can be seen in the right pulmonary artery (arrowed). (b) A 4-year-old Staffordshire Bull Terrier with caval syndrome due to heartworm disease. (bi) Left parasternal long-axis four-chamber view. A large mass of adult heartworms (H) is present in the enlarged RA. They are identified as parallel echogenic lines. (bii) Right parasternal short-axis view obtained at the level of the papillary muscles. During diastole the worms (HW) moved through the tricuspid valve and into the enlarged RV.
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9.184 The same dog as in Figure 9.183b after heartworm removal. (a) Right parasternal long-axis view. Note the enlarged RA and compare its size to that of the LA. (b) Right parasternal short-axis view obtained at the heart base and optimized for the pulmonic trunk (MPA). The MPA is enlarged both before and after the pulmonic valve. Usually, the MPA diameter is close to the diameter of the aorta (Ao) at this level. (c) M-mode obtained at the level of the papillary muscles from a right parasternal location. The RV is markedly dilated. The LV is also labelled for comparison.
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9.185 (a) Transverse (level of diaphragm) and (b) sagittal thoracic CT images of a 2-year-old neutered male mixed-breed dog diagnosed with angiostrongylosis (same dog as in Figure 9.147). There is a diffuse mild ground-glass opacity, multiple irregular regions of parenchymal consolidation and scattered ill-defined heterogeneous hyperattenuating nodular regions. These have a moderately peripheral distribution and are more severe in the caudodorsal parts of both caudal lung lobes.
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9.186 (a) Right parasternal long-axis four-chamber and (b) short-axis views of a 2-year-old neutered male mixed-breed dog with severe pulmonary hypertension associated with angiostrongylosis (same dog as in Figures 9.185 and 9.147). Marked flattening of the IVS can be seen, leading to left-sided underfilling. Dorsal to the LA, the right pulmonary artery is very dilated (arrowed).
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9.187 PTE in a 5-year-old neutered Cavalier King Charles Spaniel bitch; reason for the thromboembolism was not determined in this case. Transverse contrast-enhanced thoracic CT image showing both right and left pulmonary arteries with filling defects, consistent with large thrombi. The right heart is dilated and echocardiography confirmed presence of pulmonary hypertension. Ao = aorta; LPA = left pulmonary artery; RPA = right pulmonary artery.
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9.188 A 5-year-old neutered Cavalier King Charles Spaniel bitch (same dog as in Figure 9.187) with a large thrombus in the right pulmonary artery (RPA). (a) Right parasternal long-axis four-chamber view showing a very dilated RPA dorsal to the LA, containing a thrombus. (b) Cranial right parasternal short-axis view, optimizing the pulmonic trunk bifurcation into the pulmonary arteries. The same thrombus is visible in the RPA and a poorly defined thrombus is possibly present in the left pulmonary artery (LPA). Ao = aorta.
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9.189 (a) Post-contrast transverse CT image (soft tissue algorithm and window) of a 6-year-old neutered male Labrador Retriever with a Budd–Chiari-like syndrome due to a CdVC mass. The image was obtained caudal to the heart. The mass (M) is seen as a large soft tissue attenuating structure with a small amount of contrast medium within the CdVC ventral to it. There is also atelectasis of the ventral tip of the right caudal lung lobe. (b) A more caudal image from the same CT series. The caudal part of the mass (M) has large regions of mineralization (these were also hyperdense before contrast administration). The peritoneal effusion (E) is evident on this image, surrounding the liver lobes (L).
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9.190 Lateral angiogram of an 11-year-old neutered Labrador Retriever bitch with recurrence of severe oedema of the head, neck and thoracic limbs 1 week after removal of a thymoma. Non-selective angiography via the cephalic vein demonstrated a large intraluminal filling defect (arrowed) consistent with a thrombus in the CrVC at the level of the costocervical vein. A repeat angiogram 2 weeks later showed the thrombus to be approximately half the size. (Courtesy of D. Davies)
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9.191 Post-mortem radiograph of a dog’s heart with mineralized coronary arteries due to atherosclerosis. The dog also had hypothyroidism, which has been strongly linked with this condition.
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9.192 A cat with end-stage cardiomyopathy and biventricular CHF including small pericardial and pleural effusions. There is a very thin segment affecting most of the heart’s length to the apex, excluding the base of the LVFW. This was believed to represent a region of myocardial infarction with replacement fibrosis. (a) Right parasternal four-chamber view, showing the abrupt thinning of the LVFW (arrowed) after the basal segment. (b) Right parasternal short-axis view, showing focal thinning of the LVFW between the papillary muscles (arrowed). A cat with end-stage cardiomyopathy and biventricular CHF including small pericardial and pleural effusions. There is a very thin segment affecting most of the heart’s length to the apex, excluding the base of the LVFW. This was believed to represent a region of myocardial infarction with replacement fibrosis. (c) Left ventricular M-mode, which shows the LVFW is thin and relatively akinetic.
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9.193 Right parasternal long-axis four-chamber view of an 11-year-old neutered male Shih Tzu with thromboembolic stroke (confirmed by MRI). There is a focal hyperechoic region within the LVFW (arrowed), possibly representing a myocardial infarct. Cardiac Troponin I level was very high. The dog also had stage B1 MMVD.
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