An 8 years old, 17.1 kg, neutered female English Cocker Spaniel was presented to the cardiology service of the author’s institution for evaluation of abdominal distension. This problem, along with exercise intolerance, became apparent to the owners a week prior to presentation. In addition, a mild cough during excitement of about 2 weeks duration was reported. The referring veterinarian performed a diagnostic abdominocentesis and afterwards referred the dog to a mobile ultrasound service for an echocardiogram. Based on the results of these examinations congestive right-sided heart failure as a result of pulmonary hypertension was suspected to be the cause of the abdominal distension. Subsequently, the referring veterinarian submitted a blood sample to a veterinary laboratory for an antigen test for Angiostrongylus vasorum. This test was positive. Treatment with oral furosemide (20 mg/dog BID) and oral milbemycin (milbemycin oxime 12.5 mg with praziquantel 125 mg/dog once a week) was started. Because of the lack of clinical improvement during the first several days of therapy, the dog was referred to the cardiology service of the author’s clinic. The dog had never been to endemic areas of Dirofilaria immitis and it was not known to have had any history of trauma. At presentation the dog was bright, alert and responsive with a body condition score of 6 out of 9. Abdominal distension was apparent with a positive fluid wave. No signs of labored breathing were noticed. The respiratory rate was 24 breaths/min and the breathing pattern was costo-abdominal. The femoral pulse was moderately powerful, regular, symmetric, and without a pulse deficit, with a frequency of 108/min. Mucous membranes were pink with a capillary refill time within 1 s. A grade 4 out of 6 systolic cardiac murmur was auscultated over the right cardiac apex. No jugular venous distension was observed; however, the hepato-jugular reflux test was positive. Transthoracic echocardiography was performed using 2-dimensional, M-mode, color Doppler, pulsed wave Doppler and continuous wave Doppler techniques via the standard views [, ]. Echocardiographic examination confirmed the previously suspected severe pulmonary hypertension. A trivial amount of pericardial effusion was visible without echocardiographic signs of cardiac tamponade. The right ventricle showed severe concentric and eccentric hypertrophy. There was severe tricuspid valve regurgitation present with a systolic right ventricular to right atrial pressure gradient of 135 mmHg (reference < 31 mmHg) determined with continuous wave Doppler technique using the simplified modified Bernoulli equation [,,, ]. Two-dimensional echocardiography disclosed a flail anterior leaflet of the tricuspid valve. On this leaflet, chordal remnants could be recognized. The pulmonary trunk and the left and right pulmonary arteries showed severe uniform dilation (pulmonary trunk to aortic ratio of 1.53; reference: 0.80-1.15) and a physiologic regurgitation jet [, ]. The pulmonary artery velocity profile evaluated with pulsed wave Doppler echocardiography showed rapid rise of flow with an acceleration time of 38 ms (ref. mean 93 ± 16 ms) []. The right atrium was moderately enlarged and the interatrial septum showed bulging towards the left []. Severe systolic and diastolic flattening and paradoxical movement of the interventricular septum were noticed, which led to a severely decreased left ventricular lumen size in diastole (normalized diastolic left ventricular internal diameter of 0.62; reference: 1.27-1.85) and in systole (0.26; reference: 0.71-1.26) [, ]. The left atrium was of normal size with a left atrium to aortic ratio of 1.4; ref. </=1.6) [,, ]. No mitral regurgitation was noticed. The mitral inflow pattern showed an E-wave of 0.74 m/s (reference 0.52-0.81 m/s) and a tall A-wave of 1.79 m/s (reference 0.45-0.78 m/s) on pulsed wave Doppler examination [,, ]. The calculated pressure half-time from the mitral E-wave velocity profile was 80 ms, which was prolonged (ref. < 50 ms), suggesting a mitral valve stenosis [, ]. The systolic flow velocities within the pulmonic trunk and the aorta were within the reference ranges (1.0 and 1.2 m/s, respectively) [, ]. Focused abdominal ultrasonography showed a large amount of ascites and a marked diffuse hepatomegaly with congested hepatic veins and distended caudal vena cava without any respiratory caliber changes []. Synchronous ECG showed sinus rhythm with positive P-waves and negative QRS-complexes. Baermann larval isolation from a mixed fecal sample of three consecutive days was performed, which revealed a large number of L1 larvae of Angiostrongylus vasorum []. Fecal sedimentation and flotation techniques were negative for parasitic eggs. A serological test for circulating antigens (Angio Detect®, IDEXX) was performed from a blood sample, which was still positive. The daily oral furosemide and weekly milbemycin oxime therapies were stopped, and oral fenbendazole (50 mg/kg SID for 14 days) and oral sildenafil (1.4 mg/kg BID) tablets were prescribed and the dog was discharged. A re-check examination was scheduled in 6 weeks’ time. At the 6 weeks re-check examination the owners reported resolution of all previously noted clinical signs, such as abdominal distension, cough and exercise intolerance. Physical examination revealed a bright, alert and responsive dog, with a body condition score of 6 out of 9. The dog lost 2.6 kg in this period and weighed 14.5 kg. Abdominal distension was no longer apparent. The respiratory rate was 40 breaths/min, and the breathing pattern was costo-abdominal. The femoral pulse was moderately powerful, regular, symmetric and without a pulse deficit with a frequency of 92/min. The mucous membranes were pink with a capillary refill time less than 1 second. A grade 2 out of 6 systolic cardiac murmur was auscultated over the right cardiac apex as well as a 1 out of 6 systolic murmur with the point of maximal intensity at the mitral valve region. Transthoracic echocardiography revealed no pericardial or pleural effusion. The right ventricle still showed a severe concentric and eccentric hypertrophy. A severe tricuspid valve regurgitation was still present with a systolic right ventricular to right atrial Doppler-derived pressure gradient of 90 mmHg. The previously recognized flail tricuspid valve leaflet was still present. The pulmonary trunk and the left and right pulmonary arteries still showed a severe uniform dilation without any abnormal content (such as heartworms or thrombus). The pulmonary trunk to aorta ratio decreased (1.19) compared to the initial examination. The pulmonary artery velocity profile was unchanged with an acceleration time of 40 ms (ref. mean 93 ± 16 ms) [,, ]. The pulmonic valve showed an unchanged physiologic regurgitation jet [, ]. The right atrium was still moderately enlarged and the interatrial septum bulged towards the left atrium. Flattening of the interventricular septum was present, but was less severe than at the initial examination. The left ventricular lumen size in diastole was now normal (normalized diastolic left ventricular internal diameter of 1.29; reference: 1.27-1.85) []. The left atrium was of normal size with a left atrium to aortic ratio of 1.5; ref. </=1.6) [, ]. The mitral valve showed a diastolic doming and a moderate systolic central regurgitation jet [, ]. The mitral inflow pattern consisted of an E-wave of 1.08 m/s and an A-wave of 2.47 m/s. In addition, the E-wave showed an even longer pressure half-time (100 ms, ref. < 50 ms) than at the initial examination [, ]. Focused abdominal ultrasound examination no longer showed any peritoneal effusion. The liver was still diffusely enlarged, and the gallbladder wall was diffusely thickened, consistent with edema. The hepatic veins and the caudal vena cava were subjectively markedly distended, similarly to the initial examination. Baermann larval isolation test from a 3-day mixed fecal sample was performed, and revealed no larvae. A serological test for circulating antigens was repeated from a blood sample, and was negative. Continuation of the daily oral sildenafil (1.7 mg/kg BID) therapy was recommended until the next re-check in 2 months, and the dog was discharged. At the same time, monthly preventive moxidectin spot-on was advised for life-long use []. Two months later the owner reported via e-mail that the dog was doing excellent. Both the exercise tolerance and the abdominal size had normalized. The sildenafil was stopped 2 weeks prior to this e-mail contact, after gradual tapering of the daily dose. The owners decided against another re-check examination. However, a week later the owner reported recurrence of the abdominal distension via e-mail. An examination by the referring veterinarian confirmed the recurrence of ascites. Re-starting the sildenafil therapy (1.7 mg/kg, BID) resulted in resolution of this clinical sign within a week. After several months, the owner reduced the daily dosage of sildenafil (0.9 mg/kg, BID) due to financial reasons, which again led to recurrence of abdominal distension due to ascites. Afterwards, the daily dose was increased again (1.7 mg/kg, BID), which led to resolution of the abdominal distension. The dog was reported to be clinically healthy by the owners with daily oral sildenafil (1.7 mg/kg BID) administration 6 months after the date when eradication of French heartworm infection was confirmed with laboratory tests at the author’s institution. Thereafter, recurrence of ascites took place despite unchanged sildenafil therapy.