A 6-month-old female Kaninchen Dachshund with a tentative diagnosis of mitral valve dysplasia was referred to our center for further evaluation. The dog was smaller than its littermates and had initially presented to a veterinarian at 4 months of age due to a history of tachypnea. A cardiac murmur was auscultated, and echocardiography revealed severe mitral valve regurgitation (MR) with left ventricular and atrial enlargement. Pimobendan (0.58 mg/kg PO q12h), alacepril (3.9 mg/kg PO q12h), torasemide (0.1 mg/kg PO q12h), and isosorbide dinitrate (2.0 mg/kg PO q12h) were prescribed as treatment for MR and pulmonary edema. The patient was referred to the university animal hospital for further evaluation, where mitral dysplasia with abnormal coronary vessels was diagnosed. On presentation to JASMINE, the patient was lean with a body condition score of 4/9 and weighed 3.36 kg. A grade 3/6 left apical systolic murmur was auscultated. The femoral pulses were normal and synchronous, and lung sounds were normal in all areas. The patient was alert with a heart rate of 140 bpm, a respiratory rate of 48 breaths/min, and a temperature of 38.9 °C. Complete blood count, plasma biochemistry, and cardiac biomarker evaluation were conducted. Abnormalities detected included elevated NT-proBNP (4887 pmol/L; reference range ≤ 900 pmol/L) and ANP (259.9 pg/mL; reference range 8.6–105.8 pg/mL). Cardiac troponin I was normal (0.016 ng/mL; reference range 0.006–0.129 pg/mL). Systemic blood pressure (oscillometry) was 118/50/77 mmHg (systolic/diastolic/mean). A six-lead electrocardiography performed in the right lateral recumbency demonstrated sinus rhythm with one criterion for left ventricular enlargement (R wave amplitude of 3.1 mV in lead II). However, occasional premature ventricular contraction was observed on monitor electrocardiography during transthoracic echocardiography (TTE). The right lateral and dorsoventral thoracic radiographs revealed severe cardiomegaly (vertebral heart size, 11.6 v) [] and left atrial (LA) enlargement (vertebral left atrium size, 2.8 v) [], with no evidence of pulmonary edema. The transthoracic echocardiogram revealed severe LA dilation (2D short axis left atrial to aortic ratio 2.12) []. The left ventricle (LV) was enlarged (M-mode left ventricular internal dimension in end-diastole normalized to bodyweight 2.33) [] with mildly reduced systolic function (M-mode left ventricular internal dimension in end-systole normalized to bodyweight 1.55 [] and fractional shortening 31.5% []). However, no apparent abnormalities were observed in LV wall movement, subjectively. Color Doppler analysis was obtained through a right parasternal long-axis four-chamber view, and the mitral valve showed a moderate regurgitation signal. No structural abnormalities were found in the mitral valve complex, which consists of the mitral valve, mitral valve annulus, and papillary muscles; however, the leaflet coaptation area was decreased. The blood flow of multiple aberrant vessels was observed within the inter-ventricular septum in the right parasternal long-axis four-chamber view. Large aberrant vessels were most prominent within the LV wall and were best visualized with color Doppler. The continuous wave Doppler analysis of the aberrant vessels revealed continuous systodiastolic flow with a maximal velocity diastole (velocity, 1.20 m/s; pressure gradient, 5.76 mmHg) and a minimal velocity systole (velocity, 0.86 m/s; pressure gradient, 2.94 mmHg). The left coronary artery (LCA) optimum was not detected in the left coronary sinus, and the trunk of the coronary artery was directly connected to the PA. After these examinations, torasemide3 dosage was increased from 0.1 mg/kg PO q12h to 0.2 mg/kg PO q12h in order to reduce the volume overload. An ECG-gated CCTA of the thorax was performed under general anesthesia using a multidetector 80-row computed tomography scanner in the helical mode to obtain a detailed anatomic image of the abnormal vessels. The scanner was positioned to encompass the ascending aorta. Images were acquired at 10 and 90% of the R–R interval. Acquisition parameters of the scanning were as follows; spiral pitch factor: 0.175, tube voltage: 120 kVp, reference tube current: 250 mV, slice thickness: 0.5 mm, and a low frequency reconstruction algorithm. Contrast medium of 600 mg iodine/kg (2 mL/kg) was delivered via a power injector system into the cephalic vein at a rate of 0.7 mL/s to obtain an enhanced levophase. The examination revealed LCA and RCA originating from the PA and aorta, respectively. The dilation of RCA, LCA, and their branches; the left circumflex artery; and the left anterior descending artery were also noted. The anomalous origin of the main LCA from the PA, and prominence of the right coronary circulation with an extensive network of collaterals that communicate and supply the LCA territory were found. At the owner’s request, surgical interventions were performed 78 days after the first visit. The initial surgical plan was to use the internal thoracic artery as a bypass graft, but it was not sufficiently long to reach the left anterior descending artery (LAD). An alternative plan was applied using the left carotid artery to supply arterial blood to the LAD; the left carotid artery was dissected from the neck to the thoracic cavity and anastomosed to LAD under cardiopulmonary bypass. As the origin of LCA at the PA could not be confirmed and ligated, retrograde blood flow via LCA was recognized in the PA on post-operative echocardiography. Tachypnea resolved, but the same cardiac medications as prior to surgery was needed throughout the period after discharge since cardiomegaly did not improve. On 3 months follow-up, continuous systodiastolic flow was still observed in the aberrant vessels with no prominent changes in velocity compared to the preoperative echocardiographic values. The dog died from pulmonary edema 5 months after the surgery. Necropsy could not be performed due to lack of consent from the owner.