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Case DescriptionA two year ten month, male neutered cross breed dog presented to The Royal (Dick) School of Veterinary Studies, University of Edinburgh for evaluation of cyanosis and exercise intolerance of approximately four weeks duration. The dog had been adopted from a shelter one year previously. Exercise intolerance was associated with exertional dyspnoea and lingual cyanosis. Occasional coughing was also reported, often associated with regurgitation. The owner did not report a change or abnormality in resting or sleeping respiratory rates. On clinical examination, there was a grade II/VI systolic murmur over the left heart base and cyanosis of the lingual mucosa. The dog was panting, making evaluation of respiratory rate and effort difficult. The rest of the examination was unremarkable. Initial diagnostics included a complete blood count and serum biochemistry. Abnormalities included elevated albumin (38 g/l, reference range 26 – 35 g/l), creatine kinase (446 U/l, reference range 50 – 200 U/l) and creatinine (141 ?mol/l, reference range 40 - 132 ?mol/l). A mild hypophosphataemia was also noted (0.70 mmol/l, reference range 0.90 - 2.0 mmol/l). Arterial blood gas analysis revealed a respiratory alkalosis (pH 7.47, reference range 7.36 - 7.44), with hypocapnoea (PCO2 24 mmHg, reference range 36-44mmHg) and reduced bicarbonate (15.9 mmol/l, reference range 24.0 - 26.0 mmol/l). Severe hypoxaemia (PO2 47 mmHg, reference range 90 - 100 mmHg) was also present, corresponding to an SpO2 of 86%.Systolic blood pressure (Doppler) was 147 mmHg. A six-lead ECG demonstrated sinus rhythm with right axis deviation of the mean electrical axis. Right lateral and dorsoventral thoracic radiographs (Fig. 1a and 1b) revealed moderate cardiomegaly (vertebral heart score 12) and prominent pulmonary veins and arteries. These findings were accompanied by a large, tubular soft tissue opacity dorsal to the carina, extending from the 4th to the 8th intercostal space on the right lateral view (Fig. 1a). Cardiomegaly and the soft tissue opacity were investigated further by Doppler echocardiography. The right atrium and ventricle were severely dilated. The interventricular septum was flattened and the left ventricle was small (left ventricular internal dimension in diastole normalised to bodyweight of 1.0 (reference range 1.27 – 1.85 ADDIN EN.CITE <EndNote><Cite><Author>Cornell</Author><Year>2004</Year><RecNum>122</RecNum><DisplayText><style face="superscript">1</style></DisplayText><record><rec-number>122</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="0">122</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Cornell, C. C.</author><author>Kittleson, M. D.</author><author>Della Torre, P.</author><author>Haggstrom, J.</author><author>Lombard, C. W.</author><author>Pedersen, H. D.</author><author>Vollmar, A.</author><author>Wey, A.</author></authors></contributors><auth-address>Veterinary Medical Teaching Hospital, University of California, Davis, CA 95616-8747, USA. cccornell@ucdavis.edu</auth-address><titles><title>Allometric scaling of M-mode cardiac measurements in normal adult dogs</title><secondary-title>J Vet Intern Med</secondary-title><alt-title>Journal of veterinary internal medicine</alt-title></titles><pages>311-21</pages><volume>18</volume><number>3</number><keywords><keyword>Animals</keyword><keyword>Dogs/*physiology</keyword><keyword>Echocardiography/*veterinary</keyword><keyword>Female</keyword><keyword>Heart/*physiology</keyword><keyword>Male</keyword><keyword>*Models, Cardiovascular</keyword><keyword>Pedigree</keyword><keyword>Reference Values</keyword><keyword>Retrospective Studies</keyword></keywords><dates><year>2004</year><pub-dates><date>May-Jun</date></pub-dates></dates><isbn>0891-6640 (Print)
0891-6640 (Linking)</isbn><accession-num>15188817</accession-num><urls><related-urls><url>). A large ostium secundum atrial septal defect (ASD), measuring approximately 13mm, was identified. Interrogation with colour Doppler revealed right-to-left shunting across the defect (Video 1), which was subsequently confirmed by contrast echocardiography. The pulmonary artery was markedly dilated, with elevated flow velocity across the pulmonic valve of 2.1 m/s (reference range 1.2 ± 0.2 ADDIN EN.CITE <EndNote><Cite><Author>Kirberger</Author><Year>1992</Year><RecNum>133</RecNum><DisplayText><style face="superscript">2</style></DisplayText><record><rec-number>133</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1533648151">133</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Kirberger, R. M.</author><author>Blandvandenberg, P.</author><author>Grimbeek, R. J.</author></authors></contributors><auth-address>Univ Pretoria,Dept Stat,Pretoria 0002,South Africa</auth-address><titles><title>Doppler Echocardiography in the Normal Dog .2. Factors Influencing Blood-Flow Velocities and a Comparison between Left and Right Heart Blood-Flow</title><secondary-title>Veterinary Radiology & Ultrasound</secondary-title><alt-title>Vet Radiol Ultrasoun</alt-title></titles><periodical><full-title>Veterinary Radiology & Ultrasound</full-title><abbr-1>Vet Radiol Ultrasoun</abbr-1></periodical><alt-periodical><full-title>Veterinary Radiology & Ultrasound</full-title><abbr-1>Vet Radiol Ultrasoun</abbr-1></alt-periodical><pages>380-386</pages><volume>33</volume><number>6</number><keywords><keyword>doppler echocardiography</keyword><keyword>pulsed wave doppler</keyword><keyword>continuous wave doppler</keyword><keyword>heart rate</keyword><keyword>mass</keyword><keyword>normal</keyword><keyword>dog</keyword></keywords><dates><year>1992</year><pub-dates><date>Nov-Dec</date></pub-dates></dates><isbn>1058-8183</isbn><accession-num>WOS:A1992KC79500010</accession-num><urls><related-urls><url><Go to ISI>://WOS:A1992KC79500010</url></related-urls></urls><electronic-resource-num>DOI 10.1111/j.1740-8261.1992.tb00163.x</electronic-resource-num><language>English</language></record></Cite></EndNote>2) and unremarkable valve leaflets. There was no discernible step-up of flow velocity across the valve, suggesting a relative pulmonic stenosis i.e. secondary to volume overload, rather than a true pulmonic stenosis. There was moderate tricuspid (3.36 m/s; reference range ADDIN EN.CITE <EndNote><Cite><Author>JA</Author><Year>2011</Year><RecNum>135</RecNum><DisplayText><style face="superscript">3</style></DisplayText><record><rec-number>135</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1533650582">135</key></foreign-keys><ref-type name="Book Section">5</ref-type><contributors><authors><author>Boon JA</author></authors></contributors><titles><title><style face="normal" font="default" size="10">Hypertensive Heart Disease</style></title><secondary-title>Veterinary Echocardiography</secondary-title></titles><pages>335-350</pages><section>6</section><dates><year>2011</year></dates><pub-location>West Sussex, UK</pub-location><publisher>Wiley-Blackwell</publisher><urls></urls></record></Cite></EndNote>3) and pulmonic (3.01 m/s; reference range ADDIN EN.CITE <EndNote><Cite><Author>JA</Author><Year>2011</Year><RecNum>135</RecNum><DisplayText><style face="superscript">3</style></DisplayText><record><rec-number>135</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1533650582">135</key></foreign-keys><ref-type name="Book Section">5</ref-type><contributors><authors><author>Boon JA</author></authors></contributors><titles><title><style face="normal" font="default" size="10">Hypertensive Heart Disease</style></title><secondary-title>Veterinary Echocardiography</secondary-title></titles><pages>335-350</pages><section>6</section><dates><year>2011</year></dates><pub-location>West Sussex, UK</pub-location><publisher>Wiley-Blackwell</publisher><urls></urls></record></Cite></EndNote>3)insufficiency present, suggesting a systolic pressure gradient of ~45mmHg and diastolic pressure gradient of ~36mmHg respectively. These values were consistent with pulmonary hypertension PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5SdWRza2k8L0F1dGhvcj48WWVhcj4yMDEwPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA 4, but were presumed to underestimate pulmonary artery pressure given the dilated right atrium and hepatic venous congestion identified later using multi-detector Computed Tomography (CT). Pulmonary-systemic flow ratio (Qp:Qs) was estimated using 2D echocardiography and pulsed wave spectral Doppler. The estimated shunt ratio was 5.6, indicating a greater pulmonic vs systemic flow and significant shunting of blood ADDIN EN.CITE <EndNote><Cite><Author>M</Author><Year>2014</Year><RecNum>134</RecNum><DisplayText><style face="superscript">5</style></DisplayText><record><rec-number>134</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1533648579">134</key></foreign-keys><ref-type name="Book Section">5</ref-type><contributors><authors><author>Grossman W and Moscucci M</author></authors><secondary-authors><author>Moscucci M</author></secondary-authors></contributors><titles><title><style face="normal" font="default" size="10">Shunt Detection and Quantification</style></title><secondary-title>Grossman and Baim's Cardiac Catheterization, Angiography, and Intervention</secondary-title></titles><pages>261 - 271</pages><edition>8th</edition><section>12</section><dates><year>2014</year></dates><pub-location>Philadelphia, USA</pub-location><publisher>Lippincott Williams and Wilkins</publisher><urls></urls></record></Cite></EndNote>5. Systolic function of the right ventricle was adequate based on a tricuspid annular planar systolic excursion of 15mm ADDIN EN.CITE <EndNote><Cite><Author>Pariaut</Author><Year>2012</Year><RecNum>121</RecNum><DisplayText><style face="superscript">6</style></DisplayText><record><rec-number>121</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="0">121</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Pariaut, R.</author><author>Saelinger, C.</author><author>Strickland, K. N.</author><author>Beaufrere, H.</author><author>Reynolds, C. A.</author><author>Vila, J.</author></authors></contributors><auth-address>Department of Veterinary Clinical Sciences, LSU School of Veterinary Medicine, Baton Rouge, LA 70803, USA. rpariaut@lsu.edu</auth-address><titles><title>Tricuspid annular plane systolic excursion (TAPSE) in dogs: reference values and impact of pulmonary hypertension</title><secondary-title>J Vet Intern Med</secondary-title><alt-title>Journal of veterinary internal medicine</alt-title></titles><pages>1148-54</pages><volume>26</volume><number>5</number><keywords><keyword>Animals</keyword><keyword>Dog Diseases/*physiopathology/ultrasonography</keyword><keyword>Dogs</keyword><keyword>Echocardiography/*veterinary</keyword><keyword>Hypertension, Pulmonary/physiopathology/ultrasonography/*veterinary</keyword><keyword>Observer Variation</keyword><keyword>Reference Values</keyword><keyword>Regression Analysis</keyword><keyword>Tricuspid Valve/*physiopathology/ultrasonography</keyword><keyword>Ventricular Dysfunction, Right/physiopathology/ultrasonography/*veterinary</keyword></keywords><dates><year>2012</year><pub-dates><date>Sep-Oct</date></pub-dates></dates><isbn>1939-1676 (Electronic)
0891-6640 (Linking)</isbn><accession-num>22860631</accession-num><urls><related-urls><url>, fractional area change of the right ventricle of 35% (ref range 35.6 – 59.2 % PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5WaXNzZXI8L0F1dGhvcj48WWVhcj4yMDE1PC9ZZWFyPjxS
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ADDIN EN.CITE.DATA 7). Neither pulmonary veins nor entrance of pulmonary venous flow could be visualised on standard and non-standard views of the left atrium. A bedside ELISA test for Angiostrongylus vasorum (IDEXX Laboratories, UK), performed because of pulmonary hypertension, was negative. In order to investigate further causes of pulmonary hypertension CT angiography was performed. Contrast medium (Iomeron? 400 mg/ml Iomeprol – Bracco, Italy) was injected into the right cephalic vein (2ml/Kg, 4 ml/sec) via a power injector system (Mark V Plus? - Medrad, UK). Dextro and levo phases of the heart followed by a late phase of the thorax were performed. Moderate dilation of the right atrium and right ventricle were observed together with a generalised increased vascular pattern especially in the right hemithorax. The course taken by venous drainage from the right middle lung lobe was not clearly identifiable. The venous drainage from the other lobes merged into two distinct pulmonary veins; one from the left cranial and caudal lung lobes, and one from the right cranial, caudal and accessory lung lobes. These two vessels subsequently fused into a common large, aneurysmal, tortuous vessel that was dorsal to the mainstem bronchus (Fig. 2) and entered the right atrium via the cranial vena cava (Fig. 3). In an early dextro cardiac phase, contrast medium entering the right atrium four seconds after injection crossed the interatrial septum through the ostium secundum ASD and entered the left atrium. In the venous phase, moderate distension of the hepatic vasculature was highlighted. This was consistent with hepatic congestion upstream of elevated right atrial pressure. No other congenital abnormalities e.g. asplenia were identified based on this CT examination which was extended to include the cranial abdomen. Due to financial constraints, surgical management could not be considered. Medical management consisted of sildenafil PO (1.5 mg/kg TID) to address the pulmonary hypertension. After two months, exercise intolerance and cyanosis had become so marked that the owner requested euthanasia. On post mortem examination, there was right-sided cardiomegaly with marked right atrial dilation and severe engorgement of all the lobar branches of the pulmonary veins. The lobar branches, including the right middle vein (Fig. 4), entered two distinct left and right pulmonary veins that then merged to join a single, severely dilated pulmonary vein that communicated with the cranial vena cava before entering the right atrium. Entry of the cranial and caudal venae cavae into the right atrium was unremarkable. No pulmonary veins (left or right lobar) entered the left atrium. A 20mm wide ostium secundum ASD was present distal to the opening of the cranial vena cava within the right atrium (Fig. 5). The pulmonary artery was markedly distended (22mm wide) relative to the aorta (11mm wide), consistent with pulmonary hypertension and volume overload of the right side of the heart with relative under-loading of the left-side. This corresponds to the clinical picture and results of imaging modalities which suggested a large pulmonic flow (Qp:Qs) and dilation of pulmonary veins in the absence of left sided congestive heart failure. Overall, the findings were consistent with total anomalous pulmonary venous connection (TAPVC) ADDIN EN.CITE <EndNote><Cite><Author>Brown</Author><Year>2016</Year><RecNum>132</RecNum><DisplayText><style face="superscript">8</style></DisplayText><record><rec-number>132</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1532441517">132</key></foreign-keys><ref-type name="Book Section">5</ref-type><contributors><authors><author>Brown, DW and Geva, T</author></authors><secondary-authors><author>Allen, DH, Shaddy, RE, Penny, DJ and Feltes, TF</author></secondary-authors></contributors><titles><title>Anomalies of the Pulmonary Veins</title><secondary-title>Moss and Adams' Heart Disease in Infants, Children and Adolescents</secondary-title></titles><pages>888 - 903</pages><edition>9th</edition><section>35</section><dates><year>2016</year></dates><pub-location>Philadelphia, U.S.</pub-location><publisher>Wolters Kluwer</publisher><urls></urls></record></Cite></EndNote>8. DiscussionTAPVC is a rare congenital cardiopulmonary condition. To the author’s knowledge there are only three published reports of total anomalous pulmonary venous abnormalities in the veterinary literature, involving two dogs ADDIN EN.CITE <EndNote><Cite><Author>Hogan</Author><Year>2002</Year><RecNum>110</RecNum><DisplayText><style face="superscript">9</style></DisplayText><record><rec-number>110</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="0">110</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hogan, D. F.</author><author>Green, H. W., 3rd</author><author>Van Alstine, W. G.</author></authors></contributors><auth-address>Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907-1248, USA. dfh@vet.purdue.edu</auth-address><titles><title>Total anomalous pulmonary venous drainage in a dog</title><secondary-title>J Vet Intern Med</secondary-title><alt-title>Journal of veterinary internal medicine</alt-title></titles><pages>303-8</pages><volume>16</volume><number>3</number><keywords><keyword>Animals</keyword><keyword>Autopsy/veterinary</keyword><keyword>Dog Diseases/*pathology</keyword><keyword>Dogs</keyword><keyword>Heart Atria/abnormalities</keyword><keyword>Heart Diseases/*veterinary</keyword><keyword>Lung/*blood supply</keyword><keyword>Male</keyword><keyword>Prognosis</keyword><keyword>Pulmonary Veins/*abnormalities</keyword></keywords><dates><year>2002</year><pub-dates><date>May-Jun</date></pub-dates></dates><isbn>0891-6640 (Print)
0891-6640 (Linking)</isbn><accession-num>12043717</accession-num><urls><related-urls><url> ADDIN EN.CITE <EndNote><Cite><Author>Hilwig</Author><Year>1975</Year><RecNum>111</RecNum><DisplayText><style face="superscript">10</style></DisplayText><record><rec-number>111</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="0">111</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hilwig, R. W.</author><author>Bishop, S. P.</author></authors></contributors><titles><title>Anomalous pulmonary venous return in a Great Dane</title><secondary-title>Am J Vet Res</secondary-title><alt-title>American journal of veterinary research</alt-title></titles><pages>229-33</pages><volume>36</volume><number>2</number><keywords><keyword>Animals</keyword><keyword>Dog Diseases/*congenital/radiography</keyword><keyword>Dogs</keyword><keyword>Heart Defects, Congenital/radiography/*veterinary</keyword><keyword>Heart Septal Defects, Atrial/radiography/veterinary</keyword><keyword>Pulmonary Valve Stenosis/radiography/veterinary</keyword><keyword>Pulmonary Veins/*abnormalities</keyword></keywords><dates><year>1975</year><pub-dates><date>Feb</date></pub-dates></dates><isbn>0002-9645 (Print)
0002-9645 (Linking)</isbn><accession-num>1111390</accession-num><urls><related-urls><url> and one foal ADDIN EN.CITE <EndNote><Cite><Author>Diaz</Author><Year>2005</Year><RecNum>5</RecNum><DisplayText><style face="superscript">11</style></DisplayText><record><rec-number>5</rec-number><foreign-keys><key app="EN" db-id="st5e9s299reawve5xdaxvfxupwpzad02pzs0" timestamp="1509465237">5</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Diaz, O. S.</author><author>Desrochers, A.</author><author>Hoffmann, V.</author><author>Reef, V. B.</author></authors></contributors><auth-address>Univ Penn, New Bolton Ctr, Dept Clin Studies, Sect Sports Med & Imaging,Sch Vet Med, Kennett Sq, PA 19348 USA
Univ Penn, New Bolton Ctr, Dept Clin Studies & Pathobiol, Sch Vet Med, Kennett Sq, PA 19348 USA</auth-address><titles><title>Total anomalous pulmonary venous connection in a foal</title><secondary-title>Veterinary Radiology & Ultrasound</secondary-title><alt-title>Vet Radiol Ultrasoun</alt-title></titles><periodical><full-title>Veterinary Radiology & Ultrasound</full-title><abbr-1>Vet Radiol Ultrasoun</abbr-1></periodical><alt-periodical><full-title>Veterinary Radiology & Ultrasound</full-title><abbr-1>Vet Radiol Ultrasoun</abbr-1></alt-periodical><pages>83-85</pages><volume>46</volume><number>1</number><keywords><keyword>equine</keyword><keyword>heart and congenital cardiac anomaly</keyword><keyword>total anomalous pulmonary venous connection</keyword></keywords><dates><year>2005</year><pub-dates><date>Jan-Feb</date></pub-dates></dates><isbn>1058-8183</isbn><accession-num>WOS:000226436800017</accession-num><urls><related-urls><url><Go to ISI>://WOS:000226436800017</url></related-urls></urls><electronic-resource-num>10.1111/j.1740-8261.2005.00017.x</electronic-resource-num><language>English</language></record></Cite></EndNote>11. In all cases, juvenile animals were affected. This case report describes the use of multiple imaging modalities to diagnose TAPVC ante mortem in an adult dog. A definitive diagnosis was made post mortem. Preliminary complete blood count did not reveal evidence of secondary appropriate erythrocytosis which might be expected with severe generalised hypoxaemia as shown by lingual cyanosis and the results of the arterial blood gas ADDIN EN.CITE <EndNote><Cite><Author>Stokol</Author><Year>2017</Year><RecNum>130</RecNum><DisplayText><style face="superscript">12</style></DisplayText><record><rec-number>130</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1532428898">130</key></foreign-keys><ref-type name="Book Section">5</ref-type><contributors><authors><author>Stokol, T.</author></authors><secondary-authors><author>Ettinger, S.J, Feldman, E.C. and Etienne, C.</author></secondary-authors></contributors><titles><title>Anemia, Erythrocytosis </title><secondary-title>Textbook of Veterinary Internal Medicine</secondary-title></titles><pages>229 - 235</pages><edition>8th </edition><section>57</section><dates><year>2017</year></dates><pub-location>St. Louis, Missouri</pub-location><publisher>Elsevier</publisher><urls></urls></record></Cite></EndNote>12. The absence of polycythaemia may be related to the age of the dog as in the early stages of the disease right-to-left shunting of de-oxygenated blood may be minimal until pulmonary hypertension develops ADDIN EN.CITE <EndNote><Cite><Author>Brown</Author><Year>2016</Year><RecNum>132</RecNum><DisplayText><style face="superscript">8</style></DisplayText><record><rec-number>132</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1532441517">132</key></foreign-keys><ref-type name="Book Section">5</ref-type><contributors><authors><author>Brown, DW and Geva, T</author></authors><secondary-authors><author>Allen, DH, Shaddy, RE, Penny, DJ and Feltes, TF</author></secondary-authors></contributors><titles><title>Anomalies of the Pulmonary Veins</title><secondary-title>Moss and Adams' Heart Disease in Infants, Children and Adolescents</secondary-title></titles><pages>888 - 903</pages><edition>9th</edition><section>35</section><dates><year>2016</year></dates><pub-location>Philadelphia, U.S.</pub-location><publisher>Wolters Kluwer</publisher><urls></urls></record></Cite></EndNote>8. In dogs with right to left shunting patent ductus arteriosus erythrocytosis may not be seen until after 24 months of age ADDIN EN.CITE <EndNote><Cite><Author>Beijerink</Author><Year>2017</Year><RecNum>131</RecNum><DisplayText><style face="superscript">13</style></DisplayText><record><rec-number>131</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1532434352">131</key></foreign-keys><ref-type name="Book Section">5</ref-type><contributors><authors><author>Beijerink, N.J, Oyama, M.A, and Bonagura, J.D.</author></authors><secondary-authors><author>Ettinger, S.J, Feldman, E.C. and Etienne, C.</author></secondary-authors></contributors><titles><title>Congenital Heart Disease</title><secondary-title>Textbook of Veterinary Internal Medicine</secondary-title></titles><pages>1211 - 1217</pages><edition>8th </edition><section>250</section><dates><year>2017</year></dates><pub-location>St. Louis, Missouri</pub-location><publisher>Elsevier</publisher><urls></urls></record></Cite></EndNote>13. The remainder of the biochemical abnormalities were not specific for a right-to-left shunting cardiac anomaly. In people, TAPVC is thought to account for four-to-six per 100,000 live births . The incidence in dogs is unknown. One epidemiological study identified a single case of anomalous venous return out of 290 dogs with congenital heart disease ADDIN EN.CITE <EndNote><Cite><Author>Patterson</Author><Year>1968</Year><RecNum>119</RecNum><DisplayText><style face="superscript">15</style></DisplayText><record><rec-number>119</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="0">119</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Patterson, D. F.</author></authors></contributors><titles><title>Epidemiologic and genetic studies of congenital heart disease in the dog</title><secondary-title>Circ Res</secondary-title><alt-title>Circulation research</alt-title></titles><pages>171-202</pages><volume>23</volume><number>2</number><keywords><keyword>Angiocardiography/veterinary</keyword><keyword>Animals</keyword><keyword>*Dog Diseases/epidemiology/genetics/pathology</keyword><keyword>Dogs</keyword><keyword>Ductus Arteriosus, Patent/genetics</keyword><keyword>Female</keyword><keyword>Genes, Dominant</keyword><keyword>Heart Defects, Congenital/epidemiology/*genetics/pathology/*veterinary</keyword><keyword>Heart Septal Defects, Ventricular/genetics</keyword><keyword>Heart Valve Diseases/genetics</keyword><keyword>Male</keyword><keyword>Pedigree</keyword><keyword>Sex Factors</keyword><keyword>Tetralogy of Fallot/genetics</keyword></keywords><dates><year>1968</year><pub-dates><date>Aug</date></pub-dates></dates><isbn>0009-7330 (Print)
0009-7330 (Linking)</isbn><accession-num>5662573</accession-num><urls><related-urls><url>. Another reported one case from 976 dogs with congenital defects ADDIN EN.CITE <EndNote><Cite><Author>Oliveira</Author><Year>2011</Year><RecNum>6</RecNum><DisplayText><style face="superscript">16</style></DisplayText><record><rec-number>6</rec-number><foreign-keys><key app="EN" db-id="st5e9s299reawve5xdaxvfxupwpzad02pzs0" timestamp="1509465951">6</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Oliveira, P.</author><author>Domenech, O.</author><author>Silva, J.</author><author>Vannini, S.</author><author>Bussadori, R.</author><author>Bussadori, C.</author></authors></contributors><auth-address>Dept Cardiol, Clin Vet Gran Sasso, I-20131 Milan, Italy</auth-address><titles><title>Retrospective Review of Congenital Heart Disease in 976 Dogs</title><secondary-title>Journal of Veterinary Internal Medicine</secondary-title><alt-title>J Vet Intern Med</alt-title></titles><alt-periodical><full-title>J Vet Intern Med</full-title></alt-periodical><pages>477-483</pages><volume>25</volume><number>3</number><keywords><keyword>breed predisposition</keyword><keyword>canine</keyword><keyword>congenital heart defects</keyword><keyword>multiple heart defects</keyword><keyword>sex predisposition</keyword><keyword>patent ductus-arteriosus</keyword><keyword>pulmonic stenosis</keyword><keyword>2-dimensional echocardiography</keyword><keyword>coronary-artery</keyword><keyword>defects</keyword><keyword>valve</keyword></keywords><dates><year>2011</year><pub-dates><date>May-Jun</date></pub-dates></dates><isbn>0891-6640</isbn><accession-num>WOS:000290179100010</accession-num><urls><related-urls><url><Go to ISI>://WOS:000290179100010</url></related-urls></urls><electronic-resource-num>10.1111/j.1939-1676.2011.0711.x</electronic-resource-num><language>English</language></record></Cite></EndNote>16. It is unclear from these reports whether the cases identified were partial or total anomalous pulmonary venous connection. In children, TAPVC is repaired surgically and the outcome is ultimately dependent on whether univentricular or biventricular physiology exists. Children that undergo surgical repair of TAPVC with biventricular physiology have a better long term prognosis, with the majority living symptom- and medication-free to adulthood PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5LYXJhY2k8L0F1dGhvcj48WWVhcj4yMDEyPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA 17-19. Untreated cases in adults are rare due to advances in foetal echocardiography. However, reports of surgical correction of TAPVC in adults exist ADDIN EN.CITE <EndNote><Cite><Author>Jian</Author><Year>2012</Year><RecNum>115</RecNum><DisplayText><style face="superscript">20</style></DisplayText><record><rec-number>115</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="0">115</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Jian, X. H.</author><author>Huang, J.</author><author>Ding, Y.</author><author>Xiao, X. J.</author><author>Wu, M.</author><author>Chen, J. M.</author><author>Zhuang, J.</author></authors></contributors><auth-address>Department of Cardiovascular Surgery, Guangdong Provincial Cardiovascular Institute, Guangdong General Hospital, Guangzhou, PR China. jianxuhua@</auth-address><titles><title>Surgical outcome of isolated total anomalous pulmonary venous connection in adults: a 14-year experience</title><secondary-title>J Card Surg</secondary-title><alt-title>Journal of cardiac surgery</alt-title></titles><pages>736-9</pages><volume>27</volume><number>6</number><keywords><keyword>Adolescent</keyword><keyword>Adult</keyword><keyword>Cardiovascular Surgical Procedures</keyword><keyword>Female</keyword><keyword>Follow-Up Studies</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Retrospective Studies</keyword><keyword>Scimitar Syndrome/*surgery</keyword><keyword>Time Factors</keyword><keyword>Treatment Outcome</keyword><keyword>Young Adult</keyword></keywords><dates><year>2012</year><pub-dates><date>Nov</date></pub-dates></dates><isbn>1540-8191 (Electronic)
0886-0440 (Linking)</isbn><accession-num>23046109</accession-num><urls><related-urls><url>. Affected individuals experience clinical signs related to right-sided volume overload and right-to-left shunting, including cyanosis and heart failure. Cyanosis is normally mild and may go unnoticed in childhood. It becomes more noticeable when pulmonary hypertension develops secondary to the increased blood flow through the pulmonary vasculature, as was observed in this dog, because pulmonary hypertension promotes right-to-left shunting. TAPVC is classified according to the location of the anomalous connection with respect to the heart, and whether obstruction at the level of the pulmonary veins is present or not. There are four types of anomalous connections: supracardiac, in which the common pulmonary venous confluence drains into the superior vena cava or innominate vein, cardiac where drainage of the common pulmonary vein is into the coronary sinus, infracardiac where the common pulmonary venous confluence empties into the portal or hepatic veins, and mixed where there is drainage at two or more levels ADDIN EN.CITE <EndNote><Cite><Author>Brown</Author><Year>2016</Year><RecNum>132</RecNum><DisplayText><style face="superscript">8</style></DisplayText><record><rec-number>132</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1532441517">132</key></foreign-keys><ref-type name="Book Section">5</ref-type><contributors><authors><author>Brown, DW and Geva, T</author></authors><secondary-authors><author>Allen, DH, Shaddy, RE, Penny, DJ and Feltes, TF</author></secondary-authors></contributors><titles><title>Anomalies of the Pulmonary Veins</title><secondary-title>Moss and Adams' Heart Disease in Infants, Children and Adolescents</secondary-title></titles><pages>888 - 903</pages><edition>9th</edition><section>35</section><dates><year>2016</year></dates><pub-location>Philadelphia, U.S.</pub-location><publisher>Wolters Kluwer</publisher><urls></urls></record></Cite></EndNote>8. The most commonly reported types in people are supracardiac and cardiac PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5LYXJhY2k8L0F1dGhvcj48WWVhcj4yMDEyPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA 17, 18. The type in this case report was supracardiac. In all types of TAPVC, survival beyond the neonatal period requires a communication between the right and left sides of the heart to allow oxygenated blood to flow through the aorta. In the majority of cases an ASD or patent foramen ovale is present although patent ductus arteriosus and ventricular septal defects may also be found ADDIN EN.CITE <EndNote><Cite><Author>Brown</Author><Year>2016</Year><RecNum>132</RecNum><DisplayText><style face="superscript">8</style></DisplayText><record><rec-number>132</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1532441517">132</key></foreign-keys><ref-type name="Book Section">5</ref-type><contributors><authors><author>Brown, DW and Geva, T</author></authors><secondary-authors><author>Allen, DH, Shaddy, RE, Penny, DJ and Feltes, TF</author></secondary-authors></contributors><titles><title>Anomalies of the Pulmonary Veins</title><secondary-title>Moss and Adams' Heart Disease in Infants, Children and Adolescents</secondary-title></titles><pages>888 - 903</pages><edition>9th</edition><section>35</section><dates><year>2016</year></dates><pub-location>Philadelphia, U.S.</pub-location><publisher>Wolters Kluwer</publisher><urls></urls></record></Cite></EndNote>8. The result is a composite bidirectional shunt, where oxygenated blood from the pulmonary veins mixes with deoxygenated blood within the right atrium, and then right atrial blood shunts into the left atrium. Whether cyanosis develops is dependent on the degree of mixing of deoxygenated and oxygenated blood within the right atrium, and the volume of right atrial blood that crosses the ASD, the latter dependent on the relative compliance of right and left ventricles. Regardless of classification, affected hearts have right atrial and right ventricular dilation and hypertrophy, with a relatively normal-to-undersized left side. The pulmonary artery is also usually dilated due to pulmonary hypertension ADDIN EN.CITE <EndNote><Cite><Author>Brown</Author><Year>2016</Year><RecNum>132</RecNum><DisplayText><style face="superscript">8</style></DisplayText><record><rec-number>132</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1532441517">132</key></foreign-keys><ref-type name="Book Section">5</ref-type><contributors><authors><author>Brown, DW and Geva, T</author></authors><secondary-authors><author>Allen, DH, Shaddy, RE, Penny, DJ and Feltes, TF</author></secondary-authors></contributors><titles><title>Anomalies of the Pulmonary Veins</title><secondary-title>Moss and Adams' Heart Disease in Infants, Children and Adolescents</secondary-title></titles><pages>888 - 903</pages><edition>9th</edition><section>35</section><dates><year>2016</year></dates><pub-location>Philadelphia, U.S.</pub-location><publisher>Wolters Kluwer</publisher><urls></urls></record></Cite></EndNote>8. If pulmonary venous obstruction is present, the heart appears very similar to non-obstruction, but the person presents with pulmonary oedema early in life ADDIN EN.CITE <EndNote><Cite><Author>Brown</Author><Year>2016</Year><RecNum>132</RecNum><DisplayText><style face="superscript">8</style></DisplayText><record><rec-number>132</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1532441517">132</key></foreign-keys><ref-type name="Book Section">5</ref-type><contributors><authors><author>Brown, DW and Geva, T</author></authors><secondary-authors><author>Allen, DH, Shaddy, RE, Penny, DJ and Feltes, TF</author></secondary-authors></contributors><titles><title>Anomalies of the Pulmonary Veins</title><secondary-title>Moss and Adams' Heart Disease in Infants, Children and Adolescents</secondary-title></titles><pages>888 - 903</pages><edition>9th</edition><section>35</section><dates><year>2016</year></dates><pub-location>Philadelphia, U.S.</pub-location><publisher>Wolters Kluwer</publisher><urls></urls></record></Cite></EndNote>8. Obstruction was not present in the dog reported here. Two previous cases of total anomalous pulmonary venous abnormalities have been reported in dogs. The first was a five month old Great Dane with right sided congestive heart failure and total anomalous pulmonary venous return ADDIN EN.CITE <EndNote><Cite><Author>Hilwig</Author><Year>1975</Year><RecNum>111</RecNum><DisplayText><style face="superscript">10</style></DisplayText><record><rec-number>111</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="0">111</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hilwig, R. W.</author><author>Bishop, S. P.</author></authors></contributors><titles><title>Anomalous pulmonary venous return in a Great Dane</title><secondary-title>Am J Vet Res</secondary-title><alt-title>American journal of veterinary research</alt-title></titles><pages>229-33</pages><volume>36</volume><number>2</number><keywords><keyword>Animals</keyword><keyword>Dog Diseases/*congenital/radiography</keyword><keyword>Dogs</keyword><keyword>Heart Defects, Congenital/radiography/*veterinary</keyword><keyword>Heart Septal Defects, Atrial/radiography/veterinary</keyword><keyword>Pulmonary Valve Stenosis/radiography/veterinary</keyword><keyword>Pulmonary Veins/*abnormalities</keyword></keywords><dates><year>1975</year><pub-dates><date>Feb</date></pub-dates></dates><isbn>0002-9645 (Print)
0002-9645 (Linking)</isbn><accession-num>1111390</accession-num><urls><related-urls><url>. Diagnosis was made via angiocardiography and confirmed post mortem. The second case was an eight week old Brittany spaniel with total anomalous pulmonary venous drainage suspected after echocardiography and, again, confirmed post mortem ADDIN EN.CITE <EndNote><Cite><Author>Hogan</Author><Year>2002</Year><RecNum>110</RecNum><DisplayText><style face="superscript">9</style></DisplayText><record><rec-number>110</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="0">110</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hogan, D. F.</author><author>Green, H. W., 3rd</author><author>Van Alstine, W. G.</author></authors></contributors><auth-address>Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907-1248, USA. dfh@vet.purdue.edu</auth-address><titles><title>Total anomalous pulmonary venous drainage in a dog</title><secondary-title>J Vet Intern Med</secondary-title><alt-title>Journal of veterinary internal medicine</alt-title></titles><pages>303-8</pages><volume>16</volume><number>3</number><keywords><keyword>Animals</keyword><keyword>Autopsy/veterinary</keyword><keyword>Dog Diseases/*pathology</keyword><keyword>Dogs</keyword><keyword>Heart Atria/abnormalities</keyword><keyword>Heart Diseases/*veterinary</keyword><keyword>Lung/*blood supply</keyword><keyword>Male</keyword><keyword>Prognosis</keyword><keyword>Pulmonary Veins/*abnormalities</keyword></keywords><dates><year>2002</year><pub-dates><date>May-Jun</date></pub-dates></dates><isbn>0891-6640 (Print)
0891-6640 (Linking)</isbn><accession-num>12043717</accession-num><urls><related-urls><url>. Neither of these reports included CT in the diagnostic evaluation, which would have characterised the underlying pathology further and can facilitate surgical planning. Partial anomalous pulmonary venous connection has been described in several dogs PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5GdWppaTwvQXV0aG9yPjxZZWFyPjIwMTQ8L1llYXI+PFJl
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ADDIN EN.CITE.DATA 21-24 and one cat PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5OaWNvbHNvbjwvQXV0aG9yPjxZZWFyPjIwMTU8L1llYXI+
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ADDIN EN.CITE PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5OaWNvbHNvbjwvQXV0aG9yPjxZZWFyPjIwMTU8L1llYXI+
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ADDIN EN.CITE.DATA 25. Three of these reports detailed the use of multi-detector CT in the diagnostic evaluation PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5GdWppaTwvQXV0aG9yPjxZZWFyPjIwMTQ8L1llYXI+PFJl
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ADDIN EN.CITE.DATA 21, 23, 25, but this case describes the first application of this modality to canine TAPVC. In people, CT and MRI are routinely used to diagnose complex congenital cardiac defects. They provide detailed information about cardiac and thoracic structure and function when compared to other standard diagnostic methods such as thoracic radiographs and echocardiography. Indeed, an elegant veterinary study utilised CT and silicone endocasts to provide detailed information regarding pulmonary vein anatomy in the normal heart ADDIN EN.CITE <EndNote><Cite><Author>Brewer</Author><Year>2012</Year><RecNum>129</RecNum><DisplayText><style face="superscript">26</style></DisplayText><record><rec-number>129</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1532424756">129</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Brewer, F. C.</author><author>Moise, N. S.</author><author>Kornreich, B. G.</author><author>Bezuidenhout, A. J.</author></authors></contributors><auth-address>Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.</auth-address><titles><title>Use of computed tomography and silicon endocasts to identify pulmonary veins with echocardiography</title><secondary-title>J Vet Cardiol</secondary-title></titles><periodical><full-title>J Vet Cardiol</full-title></periodical><pages>293-300</pages><volume>14</volume><number>1</number><keywords><keyword>Animals</keyword><keyword>Dogs/*anatomy & histology</keyword><keyword>Echocardiography/*veterinary</keyword><keyword>*Models, Anatomic</keyword><keyword>Pulmonary Veins/*anatomy & histology</keyword><keyword>*Silicon</keyword></keywords><dates><year>2012</year><pub-dates><date>Mar</date></pub-dates></dates><isbn>1875-0834 (Electronic)
1760-2734 (Linking)</isbn><accession-num>22386718</accession-num><urls><related-urls><url>. Although post mortem examination was required for a definitive diagnosis in the case reported here, CT provided more anatomical information than any other imaging modality. It identified the soft tissue opacity dorsal to the carina on thoracic radiography as a large aneurysmal vessel that appeared to communicate with most of the pulmonary vessels. It also provided further characterisation of the pulmonary hypertension, making an underlying respiratory cause less likely. The only disparity between CT and post mortem findings was the path taken by the right middle pulmonary vein. On CT, there was close contiguity between the vein and the dorsal aneurysmal vein at the level of the cardiac silhouette but direct communication could not be demonstrated. Instead, it was suspected that the right middle vein emptied into the left atrium because it did not have any of the dilatory (compared to the corresponding pulmonary artery) or tortuous features of the other pulmonary veins. However, connection with the left atrium could not be demonstrated directly on CT. Post mortem examination was required to fully evaluate the path of the right middle lobar vein which merged with all the other pulmonary veins to form a large, single vein that then opened in to the right atrium. This vessel bore a striking resemblance to a scimitar vein on thoracic radiography ADDIN EN.CITE <EndNote><Cite><Author>Brown</Author><Year>2016</Year><RecNum>132</RecNum><DisplayText><style face="superscript">8</style></DisplayText><record><rec-number>132</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1532441517">132</key></foreign-keys><ref-type name="Book Section">5</ref-type><contributors><authors><author>Brown, DW and Geva, T</author></authors><secondary-authors><author>Allen, DH, Shaddy, RE, Penny, DJ and Feltes, TF</author></secondary-authors></contributors><titles><title>Anomalies of the Pulmonary Veins</title><secondary-title>Moss and Adams' Heart Disease in Infants, Children and Adolescents</secondary-title></titles><pages>888 - 903</pages><edition>9th</edition><section>35</section><dates><year>2016</year></dates><pub-location>Philadelphia, U.S.</pub-location><publisher>Wolters Kluwer</publisher><urls></urls></record></Cite></EndNote>8. However, scimitar veins are identified as part of the scimitar syndrome in people and are generally confluent with the inferior/caudal vena cava. Affected individuals often have concurrent abnormalities, including, hypoplasia of the right lung, secondary dextrocardia and hypoplasia of the right pulmonary artery ADDIN EN.CITE <EndNote><Cite><Author>Brown</Author><Year>2016</Year><RecNum>132</RecNum><DisplayText><style face="superscript">8</style></DisplayText><record><rec-number>132</rec-number><foreign-keys><key app="EN" db-id="2v25edasv9f5t8eae2b52zrqvapdwav9ptxv" timestamp="1532441517">132</key></foreign-keys><ref-type name="Book Section">5</ref-type><contributors><authors><author>Brown, DW and Geva, T</author></authors><secondary-authors><author>Allen, DH, Shaddy, RE, Penny, DJ and Feltes, TF</author></secondary-authors></contributors><titles><title>Anomalies of the Pulmonary Veins</title><secondary-title>Moss and Adams' Heart Disease in Infants, Children and Adolescents</secondary-title></titles><pages>888 - 903</pages><edition>9th</edition><section>35</section><dates><year>2016</year></dates><pub-location>Philadelphia, U.S.</pub-location><publisher>Wolters Kluwer</publisher><urls></urls></record></Cite></EndNote>8, all of which were absent in this dog. ConclusionEvaluation of dogs with evidence of right-sided volume overload and unexplained pulmonary hypertension should include advanced imaging techniques when possible. This case report describes a rare congenital condition in an adult dog in which multi-detector CT provided an accurate ante mortem diagnosis. To our knowledge this is the first veterinary case report of TAPVC diagnosed by multiple imaging modalities including multi-detector CT, and the first report of such a defect in an adult dog.Figures Figure 1a. Right lateral projection of the thorax showing moderate cardiomegaly together with a vascular pattern. A soft tissue opacity is present dorsal to the carina (*)Figure 1b. Dorsoventral radiograph of the thorax showing similar changes to the right lateral image. Figure 2. CT image showing the large dilated anomalous vessel in the dorsal thorax. RA- right atrium, CrVC-cranial vena cava.Figure 3. Reconstructed CT image showing the veins from the right caudal, left and accessory lung lobes merging before connecting to the large venous structure, which subsequently joined the right atrium via a single opening. CrVC – cranial vena cava, p.v. – pulmonary vein, Le – left, Rt – right, CD - caudal.Figure 4: Fixed tissue. Ventral view of the right lung illustrating the anomalous drainage of all right pulmonary veins into the large central vein (highlighted in red). Lobes: Cd-caudal, Acc – accessory, Mid, middle, Cr – cranial, CrVC – caudal vena cava.Figure 5: Post-mortem image demonstrating the presence of an ostium secundum ASD. RA –right atrium, ASD – atrial septal defect. VideosVideo 1Ostium secundum defectRight parasternal short axis at the level of the left atrium showing an ostium secundum defect with right-to-left shuntReferences ADDIN EN.REFLIST 1.Cornell CC, Kittleson MD, Della Torre P, Haggstrom J, Lombard CW, Pedersen HD, Vollmar A, Wey A. 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