A 26.9-kg (59.2-lb) 6-year-old spayed female German Shepherd Dog mix (dog 1) was examined after a single episode of collapse after exercise. The event had taken place 3 days prior to evaluation at the teaching hospital. Initiation of the event had not been witnessed, but the owner saw the dog lying in lateral recumbency with no apparent movement. Upon evaluation by the owner, the dog urinated, growled when assisted to rise, and was conscious but seemed disoriented. The duration of the event was estimated at < 2 minutes.
The dog's medical history included referral at 3.5 months of age for cardiovascular examination. Echo-cardiographic assessment at that time confirmed a diagnosis of valvular PAS and revealed a right ventricular outflow tract velocity of 4 m/s, equivalent to a peak systolic pressure gradient of 64 mm Hg. The dog also had a clinically significant left-to-right shunting patent ductus arteriosus and radiographie evidence of left-sided congestive heart failure. Medical treatment was initiated (furosemide, 2.4 mg/kg [1.1 mg/lb], PO, q 12 h; enalapril, 0.3 mg/kg [0.14 mg/lb], PO, q 12 h), and the ductus arteriosus was ligated without complications 10 days later via routine left thoracotomy1,2 Evaluation of radiographie views of the thorax obtained 7 days after ductal ligation indicated that congestive heart failure had resolved. Follow-up echocardiography again revealed valvular PAS, and on that occasion, outflow velocity was 4.78 m/s, corresponding to a peak right ventricular-to-PA systolic pressure gradient of 91.4 mm Hg. A dynamic component of right ventricular outflow tract obstruction associated with infundibular right ventricular hypertrophy was evident on 2-dimensional echo-cardiographic and spectral Doppler ultrasonographic imaging. Atenolol was prescribed (0.7 mg/kg [0.3 mg/ lb], PO, q 12 h) in an attempt to reduce the dynamic obstruction, and pulmonic balloon valvuloplasty was performed later, when the dog was 5 months old. Right ventricular cineangiography during the valvuloplasty procedure revealed an absence of ductal flow, moderate right ventricular hypertrophy, a thickened and stenotic pulmonary valve, poststenotic dilatation of the main PA, and patency of both PA branches (Figure 1). During the subsequent 5 years, no clinical signs referable to the cardiovascular system were seen except for 1 possible episode of exercise intolerance during a 20-minute walk. The dog was consistently medicated with atenolol at dosages that were increased according to weight. Serial echocardiographic examinations performed 1 month and 1,2, and 4 years after the valvuloplasty revealed a reduced and stable peak right ventricular-to-PA systolic pressure gradient (estimated at 65, 49, 48, and 43 mm Hg, respectively).
At the time of evaluation for exertional collapse, the dog's medication regimen consisted solely of atenolol administration (dosage, 0.46 mg/kg [0.21 mg/lb], PO, q 12 h). Physical examination at that time revealed a grade III/ VI right-sided systolic murmur and a grade II/V1 left-sided systolic murmur, heard loudest at the heart base. Both lung fields auscultated clearly Vital signs were within reference limits, and systolic arterial blood pressure obtained via Doppler oscillometry on the left forelimb was 121 mm Hg. Results of a neurologic examination were considered normal. Values from a CBC and serum biochemical analyses were within reference limits, except for mild monocy-tosis (1.9 × 109 monocytes/L; reference range, 0 to 1.2 × 109 monocytes/L) and mild hyperglobulinemia (3.5 g/dL; reference range, 2.2 to 2.9 g/dL). Serum total thyroxine concentration was normal, and results of a heartworm antigen test were negative. Thoracic radiography revealed mild right-sided cardiomegaly with prominence of the right atrium and main pulmonary trunk; the appearance of the pulmonary parenchyma was considered unremarkable. Electrocardiography revealed sinus rhythm with occasional premature ventricular complexes and a right ventricular hypertrophy pattern with a mean electrical axis of 150° in the frontal plane.
Echocardiographic evaluation revealed a normal-appearing left atrium and left ventricle. The right side of the heart had evidence of severe ventricular remodeling with a mixed-hypertrophy pattern (eg, dilatation with wall thickening). Severe right atrial enlargement was also seen, in conjunction with severe tricuspid valve régurgitation. The pulmonic valve appeared thickened and partially fused, with prominent systolic doming and poststenotic dilatation of the main PA (Figure 1). The PA branches were difficult to image, with hyperechoic tissue seen at the origin of the left PA. A stricture was suspected at the origin of the right PA. Color Doppler interrogation revealed turbulent flow in the right PA and no flow in the left PA. Turbulent flow was noticed at the level of the pulmonic valve, with a flow velocity predicting a peak right ventricular-to-PA systolic pressure gradient of 51 mm Hg. Spectral Doppler interrogation of the tricuspid valve régurgitant jet predicted a right ventricular-to-right atrial pressure gradient of 181 mm Hg. These data were interpreted as consistent with moderate valvular PAS with severe PA hypertension, likely caused by stenoses of the proximal PA branches (ie, stenosis in series). The atenolol dosage was increased (to 0.93 mg/kg [0.42 mg/ lb], PO, in the morning, and to 0.46 mg/kg, PO, in the evening), and the dog was scheduled for cardiac cath-eterization to further assess the right ventricular outflow tract and PA branches and possible means of therapeutic intervention.
Four weeks later, the dog underwent cardiac cath-eterization. At that visit, the murmurs had increased in intensity to grade IV/VI systolic on the right and grade III/VI systolic at the heart base on the left. The dog was anesthetized, and contrast transthoracic echocardiogra-phy was performed via IV injection of agitated saline (0.9% NaCl) solution to evaluate patency of the atrial septum; no flow across the atrial septum was detected. Cineangiography of the right ventricle revealed moderate to severe hypertrophy of the supraventricular crest, valvular pulmonic stenosis, dilation of the main PA, no opacification of the left PA, and a discrete 1- to 1.5-cm narrowing of the proximal portion of the right PA with poststenotic dilatation of the distal portion of the right PA (Figure 1). Pressure recordings revealed a pulmonary capillary wedge pressure of 6 mm Hg, distal right PA pressure of 21/14 mm Hg, main PA systolic pressure of 135 mm Hg, right ventricular pressure of 150/0 mm Hg, and a mean right atrial pressure of 4 mm Hg. A diagnosis of valvular PAS and peripheral PAS was made, and balloon dilation of the valve fusion was performed with a 5-cm × 25-mm balloon dilatation catheter.a The balloon catheter provided a balloon-to-annulus ratio of 0.9:1 (measured pulmonary annulus diameter, 28 mm) and was used despite being slightly undersized because no larger balloon catheters were available. A double-balloon technique may have overcome this difficulty, but the result was satisfactory with use of the single-balloon technique. Postdilatation right ventricular systolic pressure was 98 mm Hg. The dog recovered from anesthesia without complications. The following day, echocardiographic assessment revealed laminar flow across the pulmonic valve at a rate of 1.4 m/s (right ventricular-to-PA systolic pressure gradient, 7.7 mm Hg) and a tricuspid valvular régurgitant jet of 6.5 m/s (right ventricular-to-right atrial pressure gradient, 170 mm Hg), consistent with elimination of the valvular stenosis and persistence of the peripheral PAS. Recommendations were made for follow-up examination with computed tomography-assisted angiography and possible surgical palliation of the peripheral PAS. The client did not return the dog for follow-up evaluation, and contact with the referring veterinarian revealed that the dog had been euthanatized 4 months after the cardiac catheterization because of progressive syncopal events. Postmortem examination was not performed.
A 37-kg (84.1-lb) 4-year-old spayed female Golden Retriever (dog 2) was referred for evaluation of refractory seizures of 1 month's duration. Nine seizures had been seen by the owner during the 30 days prior to admission, each lasting for 30 to 90 seconds and characterized by a period of excitement prior to the event, collapse, limb rigidity, jaw clenching, and a 1-hour period of weakness or sedation afterward. Phénobarbital had been prescribed by the referring veterinarian, and the dog was being treated at a dosage of 3.5 mg/kg (1.6 mg/lb), PO, every 12 hours at the time of evaluation at the teaching hospital.
Physical examination revealed vital signs to be within reference range and a grade III/VI musical systolic ejection murmur at the heart base on the left side, with radiation to the right hemithorax. Neurologic evaluation was unremarkable. Results of a CBC, biochemical analyses, and urinalysis revealed no clinically significant abnormalities. Serum phénobarbital concentration was 24.5 μg/mL (therapeutic range, 15 to 40 μg/mL). Thoracic radiography and abdominal ultrasonography revealed no abnormalities. Echocardiography revealed normal left-sided structures and function, but a 3 × 2-cm mass was attached to and moving with the arterial surface of the pulmonic valve, resulting in moderate-to-severe acquired pulmonic valve stenosis (estimated peak right ventricular-to-PA systolic gradient, 75 mm Hg; Figure 2). The right atrium was moderately dilated, and the right ventricle had mixed hypertrophy with mild dilatation and wall thickening. These findings were consistent with valvular neoplasia, thrombus, or a sterile endocarditic vegetation. The clinical events were presumed to be syncopal and secondary to right ventricular outflow obstruction; however, a primary neurologic cause could not be excluded. Administration of aspirin (1 mg/kg [0.45 mg/lb], PO, q 12 h) was added to the treatment regimen.
Alterations in the antiepileptic regimen were made during the next 2 weeks, including addition of potassium bromide (27 mg/kg [12.3 mg/lb], PO, q 12 h) and leveteracetam (20.3 mg/kg [9.2 mg/lb], PO, q 12 h), but resulted in little change in the frequency or nature of the seizure events. Two weeks after the initial evaluation at the teaching hospital, the pulmonic valve mass was reassessed echocardiographically and was found to be unchanged in size with increased severity of the stenosis (estimated pressure gradient, 100 mm Hg). Magnetic resonance imaging of the brain was performed, with results interpreted as normal.
Because the dog did not respond to appropriate antiepileptic treatment, surgical intervention was undertaken to remove the pulmonic valve mass. In brief, mild hypothermia was induced (rectal temperature, 33.9° to 34.4°C [93° to 94°F]) and a median sternotomy was performed. The pericardium was reflected, and a fluo-ropolymer membrane patchb was sutured to the right ventricular outflow tract. The main PA and pulmonic valve annulus were incised once all venous return to the heart had been occluded, and the mass was dissected off the pulmonic valve (Figure 2). The mass was firmly adhered to the caudal wall of the PA, and excision was estimated as being 90% complete. The patch graft was closed, and venous blood flow was restored. After surgery, the dog was mechanically ventilated and remained stable until increased bleeding from the chest tube was noticed 6 hours after surgery. Blood products were administered, and the decision was made to reexplore the thorax, but the dog developed cardiac arrest prior to surgical exploration. An attempt at open-thorax resuscitation was unsuccessful. On postmortem examination, the patch graft appeared well-adhered to the epicardial surface, and a cause for the postoperative hemorrhage was not readily apparent. Results of histologie evaluation of the mass and the remaining tissue in the main PA were consistent with an intracardiac fibrosarcoma arising from the distal surface of the pulmonic valve.
A 5-kg (11-lb) 14-week-old female Pembroke Welsh Corgi (dog 3) was evaluated on a referral basis because of a patent ductus arteriosus. The dog had undergone surgery for the patent ductus approximately 2 weeks previously at a local veterinary clinic. The dog's pre- and postoperative clinical status had been unremarkable. On physical examination, a grade V/ VI continuous murmur was detected at the heart base on the left side. Thoracic radiography revealed moderate left atrial and ventricular enlargement, severely decreased vascularity in the left hemithorax with partial atelectasis of the left lung, overcirculation and increased vascularity in the right hemithorax, and no evidence of pulmonary edema (Figure 3). Echocar-diographic imaging revealed moderate left atrial and ventricular dilatation with preserved systolic function, continuous turbulent flow entering the main PA consistent with a left-to-right shunting patent ductus arteriosus, and focal constriction at the origin of the left PA with dilatation of the left PA distal to this constriction. It was not possible to interrogate flow and obtain the pressure gradient across the stenotic left PA because of contamination by the ductal flow signal. However, the velocity of the ductal flow (systolic velocity of 5 m/s corresponding to an aorta-to-PA pressure gradient of 100 mm Hg) predicted normal main PA systolic pressure. These findings were suggestive of left PA ligation during the prior surgery and continued patency of the ductus arteriosus. The thorax was explored via left lateral thoracotomy at the fourth intercostal space. A consolidation of granulation tissue was seen overlying the heart base and great vessels and was bluntly dissected with minor associated bleeding. The patent ductus arteriosus was isolated and double ligated with size-0 polypropylene suture materials Remnants of suture material from the prior surgery were seen caudal to the ductus arteriosus, although the anatomic location of these sutures was not readily apparent. Further dissection of the suture remnants was not possible given the concern about hemorrhage. Surgical closure was routine, and the dog recovered from anesthesia without complications.
The dog remained clinically normal after surgery, and ovariohysterectomy was performed without complications 4 months later. Thoracic radiography and echocardiography 3.5 years after the initial surgery revealed persistent stenosis of the left PA and reduced vascularity in the left hemithorax.
An H-kg (24.3-lb) 13.5-year-old castrated male Boston Terrier (dog 4) was evaluated for abdominal distension and suspected cardiac disease. Distention of the abdomen had been noticed by the owners for 1 week. The medical history was unremarkable except for chronic mild rectal prolapse and year-round administration of milbemycin oximed for heartworm prevention.
On physical examination, sinus tachycardia and a heart rate as high as 160 beats/min were detected in conjunction with a grade III/V1 left apical systolic murmur and a grade II/VI systolic murmur at the apex on the right side. Occasional premature beats and an intermittent gallop rhythm were auscultated. Palpation of the abdomen revealed a prominent abdominal fluid wave and moderate hepatomegaly. Cytologie analysis of an abdominal fluid sample obtained via abdominocentesis indicated that the fluid was a modified transudate, with a nucleated cell count of 1,450 WBCs/μL. and protein concentration of 4.5 g/dL. Serum biochemistry values were within reference range. An ECG revealed frequent premature atrial complexes, occasionally in bigeminal distribution. Thoracic radiography revealed a rounded soft tissue mass separate from and silhouetting with the left cranial margin of the cardiac silhouette that was causing dorsal and rightward deviation of the trachea; mild pleural effusion; and enlargement of the right ventricle, left ventricle, and left atrium (Figure 4). Echocardiography revealed a 4.8 × 5.8-cm mass of mixed echogenicity at the heart base that was partially compressing the dorsal wall of the left atrium. The main PA was observed in close proximity to the mass, with both PA branches surrounded by suspected neoplastic tissue. Acceleration of flow out both the left and right PAs was confirmed on both color and spectral Doppler ultrasonographic imaging. Moderate right ventricular and right atrial enlargement with a prominent central jet of tricuspid valve régurgitation were seen; the 4.18 m/s velocity of the tricuspid valve régurgitant flow was predictive of high right ventricular systolic pressures (estimated peak right ventricular-to-right atrial systolic pressure gradient, 70 mm Hg). Both atrioventricu-lar valves were moderately thickened and had changes compatible with degenerative valve disease (ie, endocardiosis). Mild mitral valve régurgitation and left atrial enlargement were noticed. The pulmonary veins were difficult to image and were in close proximity to the mass but appeared patent with laminar flow of blood into the left atrium.
A tentative diagnosis of heart base neoplasia with external compression of the PA branches and resultant precapillary PA hypertension and right-sided heart failure was made. The dog was discharged to the owner's care on medical treatment that included fu-rosemide (2.3 mg/kg [1 mg/lb], PO, q 12 h), enalapril (0.23 mg/kg [0.1 mg/lb], PO, q 12 h), and spironolactone (1.1 mg/kg [0.5 mg/lb], PO, q 12 h). This treatment regimen did not fully control accumulation of ascites fluid, and therapeutic abdominocentesis was performed by the referring veterinarian every 2 to 4 weeks.
The dog was reevaluated 4 months after initial diagnosis. Substantial weight loss of 1.6 kg (3.5 lb) and dorsal muscle wasting had developed during the preceding 4 months. The dog had mild dyspnea and exercise intolerance secondary to peritoneal fluid accumulation, which resolved after abdominocentesis. At that visit, respiratory rate, blood pressure, and heart rate were within normal limits; normal sinus rhythm was auscultated; and renal variables indicated only mildly high values for SUN concentration (29 mg/dL; reference range, 5 to 20 mg/dL). Echocardiography revealed minimal change in the size of the mass (4.6 × 6.3 cm) and persistence of PA stenosis. An estimate of right ventricular systolic pressure made on the basis of tricuspid valve régurgitant flow velocity was comparable to the initial pressure (right ventricular-to-right atrial systolic pressure gradient, 66 mm Hg). The treatment regimen was altered by increasing the furosemide dosage (2.7 mg/kg [1.2 mg/lb], PO, q 8 h), adding an injectable furosemide treatment (2.7 mg/kg, SC, q 48 h), and supplementing omega-3 fatty acids (38.3 mg/kg [17.4 mg/lb], PO, q 24 h of eicosapentaenoic acid; 25.5 mg/ kg [11.6 mg/lb], PO, q 24 h of docosahexaenoic acid). At the time of manuscript preparation (9 months after initial diagnosis), the dog remained stable on this regimen with therapeutic abdominocentesis required every 2 weeks, although progressive cachexia and weight loss had developed despite normal appetite.
Pulmonary artery stenosis
NuMED Inc, Hopkinton, NY.
Gore-Tex, WL Gore & Associates Inc, Flagstaff, Ariz.
Prolene, Ethicon Inc, Somerville, NJ.
Interceptor, Novartis Animal Health US Inc, Greensboro, NC.
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