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Objectives: To describe a series of dogs with pulmonary artery dissection and patent ductus arteriosus (PDA)., Animals: Eight dogs., Methods: Retrospective case series., Results: Pulmonary artery dissection was diagnosed in 8 dogs, 3 were Weimaraners. Four dogs presented in left-sided congestive heart failure, 4 presented for murmur evaluation and without clinical signs, and 1 presented in right-sided congestive heart failure. In 7 dogs the dissection was first documented concurrent with a diagnosis of uncorrected PDA. In the other dog, with pulmonary valve stenosis and PDA, the dissection was observed on autopsy examination 17 months after balloon pulmonary valvuloplasty and ductal closure. Median age at presentation for the 7 dogs with antemortem diagnosis of pulmonary artery dissection was 3.5 years (range, 1.5-4 years). Three dogs had the PDA surgically ligated, 2 dogs did not undergo PDA closure, 1 dog failed transcatheter occlusion of the PDA with subsequent surgical ligation, 1 dog underwent successful transcatheter device occlusion of the PDA, and 1 dog had the PDA closed by transcatheter coil delivery 17 months prior to the diagnosis of pulmonary artery dissection. The 2 dogs that did not have the PDA closed died 1 and 3 years after diagnosis due to heart failure., Conclusions: Pulmonary artery dissection is a potential complication of PDA in dogs, the Weimaraner breed may be at increased risk, presentation is often in mature dogs, and closure of the PDA can be performed and appears to improve outcome., (Copyright © 2014 Elsevier B.V. All rights reserved.)

This study was designed to evaluate the feasibility and limitations of transcatheter embolization coil occlusion of patent ductus arteriosus in dogs using a carotid artery approach. Seven dogs examined at the University of California, Davis Veterinary Medical Teaching Hospital in 2002-2003 for evaluation of heart disease had congenital patent ductus arteriosus diagnosed by characteristic physical, electrocardiographic, radiographic, and anatomic and Doppler echocardiographic findings. Dogs were anesthetized for transesophageal echocardiography and transcatheter coil embolization of the ductus via the right external carotid artery. Coil embolization was achieved in all seven cases, using one to four detachable embolization coils. There were no major complications. Minor complications occurred in two dogs (additional coils placed using a femoral arterial approach and coil embolization of a left femoral artery branch). One dog was examined only 24 h post-operatively and had no murmur and trivial residual ductal flow by Doppler echocardiography. The other 6 dogs were clinically healthy when examined up to three years post-intervention. One dog had a very soft continuous murmur and mild residual ductal flow; the other five had no audible continuous murmur, with only one dog having trivial residual ductal flow identified by Doppler echocardiography. Although technically challenging, coil embolization via the carotid artery is a viable alternative approach for transcatheter closure of patent ductus arteriosus in some dogs.

The first case of canine endocarditis caused by "Bartonella rochalimae" is reported. By PCR-restriction fragment length polymorphism, sequence, and phylogenetic analyses, Bartonella isolates from a dog with endocarditis, 22 gray foxes, and three dogs, described as B. clarridgeiae like, were confirmed to belong to the new species "B. rochalimae," suggesting canids as the natural reservoir.

We reviewed the indications for age and breeds of dogs who received transvenous endocardial artificial pacemaker (AP) implantation (n = 105) and complications and survival thereafter at a single institution over a 6-year period. A third-degree atrioventricular (AV) block (59%) and sick sinus syndrome (SSS; 27%) were the most common indications, along with a high-grade second-degree AV block (9%) and atrial standstill (5%). The most common breeds identified were Labrador Retriever (n = 16; 11 with a third-degree AV block), American Cocker Spaniel (n = 14; 10 with SSS), and Miniature Schnauzer (n = 13; all with SSS). Common presenting complaints were syncope (n = 66) and exercise intolerance or lethargy (n = 25). Half of the dogs (n = 52) had a history of acute onset of clinical signs (<2 weeks). Mean survival time for the 60 dogs who died during the study period was 2.2 years (range, 0.1-5.8 years). Major complications occurred in 13% of dogs and included lead displacement (n = 7), sensing problems that led to syncope (n = 3), infection at the pacemaker site (n = 1), bleeding (n = 1), and ventricular fibrillation during implantation (n = 1; successfully defibrillated). Minor complications occurred in 11 dogs (11%). The success rate of transvenous AP implantation was comparatively high (all dogs survived the first 48 hours), and the complication rate was comparatively low when compared with a previous multicenter study, most likely because of how commonly the procedure was performed and supervisory experience.

Records from dogs (n = 125) that underwent attempted transarterial coil occlusion of patent ductus arteriosus (PDA) at the University of California, Davis, between 1998 and 2003, were reviewed, and a subset of these dogs (n = 31) in which the procedure was performed at least 12 months earlier were reexamined to determine long-term outcome. Coil implantation was achieved in 108 dogs (86%). Despite immediate complete ductal closure in only 34% of dogs, the procedure was hemodynamically successful as evidenced by a reduction in indexed left ventricular internal diameter in diastole (LVIDd; P < .0001), fractional shortening (P < .0001), and left atrial to aortic ratio (LA: Ao; P = .022) within 24 hours. Complete ductal closure was documented in 61% of dogs examined 12 to 63 months after coil occlusion. Long-standing residual ductal flow in the other 39% of dogs was not associated with increased indexed LVIDd or LA: Ao and was not hemodynamically relevant. Repeat intervention was deemed advisable in only 4 dogs with persistent (n = 1) or recurrent (n = 3) ductal flow. Complications included aberrant embolization (n = 27), death (n = 3), ductal reopening (n = 3), transient hemoglobinuria (n = 2), hemorrhage (n = 1), aberrant coil placement (n = 1), pulmonary hypertension (n = 1), and skin abscessation (n = 1). Serious infectious complications did not occur despite antibiotic administration to only 40% of these dogs. Transarterial coil occlusion was not possible in 14 dogs (11%) because of coil instability in the PDA and was associated with increased indexed minimum ductal diameter (P = .03), LVIDd (P = .0002), LVIDs (P = 0.001), and congestive left heart failure (P = .03) reflecting a relatively large shunt volume.

Membranous ventricular septal aneurysm was diagnosed by echocardiography in 17 dogs and three cats. The aneurysm appeared as a thin membrane protruding into the right ventricle from the margins of a congenital ventricular septal defect (VSD). The aneurysm was intact in nine dogs and two cats and perforated by a small VSD in eight dogs and one cat. Other congenital heart defects were present in seven dogs. In all animals, the aneurysm was an incidental finding observed during echocardiographic examination, and it did not appear to directly cause any cardiac dysfunction.

A prospective study was performed (June 1999 to May 2001) to determine the incidence of infective endocarditis (IE) due to Bartonella in dogs in northern California and to compare these patients with other dogs with IE. IE was diagnosed antemortem based on clinical signs and echocardiography in 18 dogs. The etiologic agent was Bartonella sp. in 5 dogs (28%) and was diagnosed by high seroreactivity to Bartonella (titer > 1:512; range, 1:1,024-1:4,096); and confirmed postmortem by positive polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) from the infected valve and partial DNA sequencing of the citrate synthase gene (glt A). Conventional bacteria were causative agents in 7 dogs (39%). An etiologic agent was not identified in 6 dogs (33%). Bartonella vinsonii berkhoffii (n = 3), B clarridgeiae (n = 1), and a B clarridgeiae-like organism (n = 1) were identified. Blood culture was positive only for the IE case due to B clarridgeiae. All dogs with IE due to Bartonella were also seroreactive to Anaplasma phagocytophilum. All dogs with IE due to Bartonella had lesions only on the aortic valve. Of the cases of IE not due to Bartonella, 31% involved the aortic valve, 61% the mitral valve, and 8% both valves. Dogs with mitral valve IE lived longer than all dogs with aortic valve IE (P = .004) and dogs with IE of the aortic valve due to Bartonella (P = .002). In conclusion, Bartonella is a common cause of IE in dogs of northern California. A high Bartonella serologic titer (> 1:512) is useful antemortem to diagnose aortic valve IE due to Bartonella.

Echocardiographic studies from 50 dogs with congenital subaortic stenosis were examined. The degree of concentric, left-ventricular hypertrophy as assessed by M-mode measurement demonstrated a positive relationship (P<0.05) to disease severity. However, the clinical utility of these measures is hindered by a large amount of individual variation (r2=0.243 to 0.473). Two-dimensional ultrasound was used to compare the cross-sectional area of the left-ventricular outflow tract to the cross-sectional area of the aortic root. The ratio of these two areas demonstrated a strong inverse relationship (P=0.001; r2=0.778) with disease severity. This ratio provides a method of estimating severity of disease by two-dimensional echocardiography.

We report the first documented case of endocarditis associated with Bartonella clarridgeiae in any species. B. clarridgeiae was identified as a possible etiological agent of human cat scratch disease. Infective vegetative valvular aortic endocarditis was diagnosed in a 2.5-year-old male neutered boxer. Historically, the dog had been diagnosed with a systolic murmur at 16 months of age and underwent balloon valvuloplasty for severe valvular aortic stenosis. Six months later, the dog was brought to a veterinary hospital with an acute third-degree atrioventricular block and was diagnosed with infective endocarditis. The dog died of cardiopulmonary arrest prior to pacemaker implantation. Necropsy confirmed severe aortic vegetative endocarditis. Blood culture grew a fastidious, gram-negative organism 8 days after being plated. Phenotypic and genotypic characterization of the isolate, including partial sequencing of the citrate synthase (gltA) and 16S rRNA genes indicated that this organism was B. clarridgeiae. DNA extraction from the deformed aortic valve and the healthy pulmonic valve revealed the presence of B. clarridgeiae DNA only from the diseased valve. No Borrelia burgdorferi or Ehrlichia sp. DNA could be identified. Using indirect immunofluorescence tests, the dog was seropositive for B. clarridgeiae and had antibodies against Ehrlichia phagocytophila but not against Ehrlichia canis, Ehrlichia ewingii, B. burgdorferi, or Coxiella burnetii.

The demographics and natural clinical history of canine congenital subaortic stenosis (SAS) were evaluated by retrospective analysis of 195 confirmed cases (1967 to 1991), 96 of which were untreated and available for follow-up evaluation. Of these, 58 dogs had left ventricular outflow systolic pressure gradients available for assessment of severity. All 195 dogs were used for demographic analysis. Breeds found to be at increased relative risk included the Newfoundland (odds ratio, 88.1; P < .001), Rottweiler (odds ratio, 19.3; P < .001), Boxer (odds ratio, 8.6; P < .001), and Golden Retriever (odds ratio, 5.5; P < .001). Dogs with mild gradients (16 to 35 mm Hg) and those that developed infective endocarditis or left heart failure were diagnosed at older ages than those with moderate (36 to 80 mm Hg) and severe (> 80 mm Hg) gradients. Of 96 untreated dogs, 32 (33.3%) had signs of illness varying from fatigue to syncope; 11 dogs (11.3%) developed infective endocarditis or left heart failure. Exercise intolerance or fatigue was reported in 22 dogs, syncope in 11 dogs, and respiratory signs (cough, dyspnea, tachypnea) in 9 dogs. In addition, 21 dogs (21.9%) died suddenly. Sudden death occurred mainly in the first 3 years of life, primarily but not exclusively, in dogs with severe obstructions (gradient, > 80 mm Hg; odds ratio, 16.0; P < .001). Infective endocarditis (6.3%) and left heart failure (7.3%) tended to occur later in life and in dogs with mild to moderate obstructions.(ABSTRACT TRUNCATED AT 250 WORDS)

Intrapericardial cysts were identified as the cause of impaired cardiac filling in six young dogs. Pneumopericardiography and two-dimensional echocardiography showed the cysts in 2 of 2 dogs and in 4 of 4 dogs, respectively. One dog, which was also infected with heartworms, died before surgical excision of the cyst could be performed. In the remaining dogs, surgical excision of the cysts and subtotal pericardiectomy was successfully accomplished. Histologic examination of the excised tissue from one dog suggested that it was a pericardial coelomic cyst. The gross and histologic characteristics of the cysts removed from the other five dogs resembled those of acquired cystic hematomas. The etiopathogenesis of these cysts was uncertain, but all cysts were connected to a fatty pedicle of tissue. In one dog, a stalk of tissue was observed to enter the pericardium through a small peritoneopericardial diaphragmatic hernia. In four dogs, the stalk of tissue was adhered to the apex of the parietal pericardium. These observations suggested that intrapericardial cysts, in some dogs, develop in association with, and possibly as a result of, congenital herniation and entrapment of omentum or a portion of the falciform ligament into the pericardial sac.

Balloon dilation during cardiac catheterization was evaluated for the treatment of congenital subaortic stenosis (SAS) in nine dogs. Under general anesthesia, bilateral cardiac catheterization was performed through the right jugular vein and carotid artery. Thermodilution cardiac output, and left ventricular and aortic root pressures and angiograms were obtained before and after balloon dilation. Balloons measuring 18-20 mm in diameter and 30-40 mm in length were positioned across the stenosis and three inflations 4-5 minutes apart were performed. There was no significant change in cardiac output, aortic pressure, or degree of aortic regurgitation after balloon dilation. For the entire group balloon dilation resulted in significant decreases in left ventricular systolic pressure (-61.2 +/- 37.2 mm Hg [mean change +/- SD], range -14 to -123), mean systolic pressure gradient (-39.6 +/- 24.4 mm Hg, range -8.4 to -72.2), and peak systolic pressure gradient (-64.3 +/- 46.5 mm Hg, range -17 to -143). Calculated left ventricular outflow cross-sectional area increased significantly (+.4 +/- .5 cm2, range -.06 to + 1.30). Clinical signs improved in the five symptomatic dogs. Individual hemodynamic responses varied widely, but the magnitude of improvement correlated with the severity of obstruction. Three dogs showed a decrease of 60% or greater (> or = 100 mm Hg), and six dogs showed a decrease of 25-50% (17-71 mm Hg) in peak systolic gradient after balloon dilation. Complications were frequent but most were transient and manageable. These preliminary results suggest that balloon dilation can acutely decrease outflow resistance in dogs with SAS and may be effective therapy for some affected dogs.

Cor triatriatum dexter is a congenital heart defect in which the embryologic right sinus venosus valve persists as a septum within the right atrium. Cor triatriatum dexter was diagnosed in 2 dogs on the basis of clinical signs, two-dimensional echocardiography, and cardiac catheterization. In 1 of the dogs, the condition was successfully treated by surgical resection of the intra-atrial septum. In the second dog, the defect was associated with an incomplete persistent cranial left vena cava and Ebstein's anomaly; surgery was declined.

Permanent transvenous cardiac pacemakers were implanted in 40 dogs. Electrocardiographic diagnoses included persistent atrial standstill (3 dogs), sick sinus syndrome (8 dogs), and high-grade second-degree or third-degree atrioventricular (AV) block (29 dogs). Thirteen dogs were alive and well 4 to 42 months after pacemaker implantation (mean, 16.9 months). The mean and median survival times of the 26 dogs that died or were euthanatized during the study were 17.9 months and 13 months, respectively. Most of these dogs succumbed to problems unrelated to the arrhythmia and pacemaker implant. One dog was lost to follow-up. Complications associated with permanent transvenous pacemaker implantation included lead dislodgement, infection, hematoma formation, skeletal muscle stimulation, ventricular arrhythmia, migration of the pulse generator, and skin erosion. Lead dislodgement was the most common complication, occurring in 7 of 9 dogs paced using untined electrode leads and in 6 of 30 dogs paced using tined leads. Lead dislodgement did not occur in the only dog paced using an actively fixed endocardial lead. It was concluded that permanent transvenous cardiac pacing is a feasible, less traumatic alternative to epimyocardial pacing in dogs, but that successful use of this technique requires careful implantation technique and anticipation of the potential complications.

Seven dogs with pulmonary lymphomatoid granulomatosis were reviewed. The disease occurred in six large-breed and one small-breed dogs. The dogs were five to 14 years old (mean, 8.4; median, 7), and four of seven dogs were males. Three dogs had been previously treated with adulticide therapy for canine dirofilariasis. Clinical histories included a progressive respiratory disease characterized by varying degrees of cough, dyspnea, exercise intolerance, and weight loss. Thoracic radiographic features included hilar lymphadenopathy, pulmonary masses of varying sizes, and mixed pulmonary patterns of lobar consolidation with ill-defined interstitial and alveolar pulmonary infiltrates. Cardiovascular changes compatible with chronic dirofilariasis were present in three dogs. The clinical course was usually progressive and fatal. The survival time ranged from six days to four years (mean, 12.5 mos; median, 3 mos). Gross and histologic features included mass lesions with areas of necrosis that replaced normal pulmonary architecture. Cytologically, these lesions were characterized by infiltration with pleomorphic, angioinvasive mononuclear cells that often resulted in vascular obliteration. The infiltrating cells resembled large lymphoid cells that possessed large hyperchromatic nuclei and small amounts of cytoplasm. Systemic lymphoid neoplasia with peripheral lymphadenopathy was diagnosed in two dogs. In both cases, lymph-node cytology was similar to the cellular infiltrates found in the lungs and consistent with a diagnosis of lymphomatoid granulomatosis. These features are compared with previously reported cases of canine lymphomatoid granulomatosis and those features identified in a similar disease described in man.

The clinicopathologic features of constrictive pericardial disease in 13 dogs were reviewed. The causes were infection (3 dogs), metallic foreign body (1 dog), and idiopathic (9 dogs). Owner complaints included abdominal enlargement, tachypnea, weakness or syncope, exertional fatigue, and weight loss. Ascites and jugular venous distention were consistently observed, whereas abnormalities of arterial pulses and heart sounds were variable and inconsistent. Diminished QRS voltages were common. Mild to moderate cardiomegaly, rounding of the cardiac silhouette, and variable and nonspecific angiographic findings were frequently observed. Cardiac catheterization consistently showed elevation and equilibration of atrial and ventricular diastolic pressures, but a prominent early diastolic (y) descent was uncommon. Fibrosis was confined to the parietal pericardium in 8 dogs, and included the epicardium in 5 dogs. Parietal pericardectomy was successful in relieving the syndrome in 6 of 10 dogs. Pulmonary thrombosis was the most common cause of early postoperative mortality.

The physical, chemical, and cytologic characteristics of 50 pericardial effusions were reviewed to determine their value to the clinician for distinguishing a variety of pericardial disorders in the dog. Pericardial fluid analysis allowed identification of chylous and bacterial pericardial effusions. Overlap in the ranges of RBC counts, nucleated cell counts, and protein concentrations between dogs with neoplastic and nonneoplastic disorders precluded identification of the cause of the effusion. Of 19 neoplastic effusions, 74% were not detected on the basis of cytologic findings and 13% of 31 nonneoplastic effusates were falsely reported as positive or suspect for a neoplasm. It was concluded that pericardial fluid analysis, including cytologic examination, did not reliably distinguish neoplastic from nonneoplastic disorders.

The hemodynamics of progressive pneumopericardium were studied in 6 anesthetized healthy dogs (with intact thorax). Heart rate, cardiac output, and pericardial and intravascular pressures were recorded. Pressures were measured in the pericardial space by means of a percutaneously introduced, air-filled catheter, and in the right atrium, right ventricle, left atrium, left ventricle, pulmonary artery, and aorta by means of fluid-filled catheters. The gradual increase in mean pericardial pressure up to 11 +/- 2 mm of Hg was associated with increases in heart rate and mean right atrial, mean left atrial, right ventricular end-diastolic, and left ventricular end-diastolic pressures and with decreases in cardiac output and stroke volume, with no change in left ventricular systolic and mean aortic pressures. Critical cardiac tamponade occurred at a pericardial pressure of 12.2 +/- 2.8 mm of Hg, which was produced by 8.7 +/- 1.9 cm3 air/kg of body weight. This was characterized by a sudden marked decrease in heart rate, cardiac output, stroke volume, left ventricular systolic pressure, and mean aortic pressure, and equilibration of mean right atrial, mean left atrial, right ventricular end-diastolic, left ventricular end-diastolic, and pulmonary artery diastolic pressures. These hemodynamic changes were similar to those of experimental pericardial effusion.

The clinical features of endocarditis of the aortic valve in 24 dogs were reviewed. This condition was found most commonly in large-breed, middle-aged male dogs. Evidence of antecedent infection or immunosuppression was usually not historically verified or found at necropsy. However, an association with congenital heart disease, especially discrete subaortic stenosis, was demonstrated. The most frequent clinical findings were systolic and diastolic murmurs and bounding arterial pulses, with or without signs of congestive heart failure. The most commonly isolated organisms were Corynebacterium sp, Erysipelothrix rhusiopathiae, and Streptococcus sp. In addition to antibiotic therapy, treatment for congestive heart failure often was required. Despite aggressive therapy, most affected dogs died as a result of congestive heart failure, arrhythmias, infarction, sepsis, or renal failure.

Ninety dogs naturally infected with Dirofilaria immitis and 103 noninfected dogs, as determined by necropsy, were used to compare the sensitivity and specificity of the cuticular and somatic reactions of the indirect fluorescent antibody test (IFA-C and IFA-S, respectively) and 2 enzyme-linked immunosorbent assays (ELISA). In microfilaremic and amicrofilaremic heartworm-infected dogs, negative results were common for all serotests. In dogs without adult heartworms at necropsy, 32% to 49% were positive, using 1 ELISA, 27% to 29% were positive with the other ELISA, 15% to 36% were positive with the IFA-S, and 0% to 1% were positive using the IFA-C, depending on the classification of borderline reactions. The prevalence of false positive serotests was probably not due to the detection of precardial stages of D immitis in dogs obtained from areas of low endemicity. Until the causes of the false-positive tests are resolved, the use of currently available serotests for routine diagnostic screening or as criteria for instituting treatment is not recommended.