Paroxysmal atrial fibrillation in seven dogs with presumed neurally-mediated syncope.

OBJECTIVES: To document the electrocardiographic findings of vagally-induced paroxysmal atrial fibrillation following a presumed reflex syncopal episode in the dog. ANIMALS: Seven dogs with a syncopal episode followed by a paroxysm of atrial fibrillation recorded on a 24-hour Holter. METHODS: Twenty-four hour Holter monitors were retrospectively reviewed, analysing the cardiac rhythm associated with syncopal events. Each recording was analysed from 10 min before the syncopal episode to until 10 min after a normal sinus rhythm had returned. RESULTS: Nine episodes were recorded in seven dogs, with one patient experiencing three events during one Holter recording. Five of the seven dogs presented with underlying structural heart disease. In two the syncopal episodes occurred following exercise, two associated with coughing and three were during a period of rest. All dogs had documented on the Holter recording a rhythm abnormality during syncope. The most common finding leading up to the syncopal event was development of a progressive sinus bradycardia, followed by sinus arrest interrupted by a ventricular escape rhythm and then ventricular arrest. This was then followed by an atrial fibrillation. The atrial fibrillation was paroxysmal in seven recordings and persistent in two. In two dogs, the atrial fibrillation reorganised into self-limiting runs of atypical atrial flutter. CONCLUSIONS: This combination of electrocardiographic arrhythmias are probably caused by an inappropriate parasympathetic stimulation initiating a reflex or neurally-mediated syncope, with abnormal automaticity of the sinus node and of the subsidiary pacemaker cells and changes in the electrophysiological properties of the atrial muscle, which promoted the paroxysmal atrial fibrillation.

Outcome in 55 dogs with pulmonic stenosis that did not undergo balloon valvuloplasty or surgery.

OBJECTIVE: To determine the outcome, independent predictors of cardiac death, and the Doppler-derived pressure gradient cut-off for predicting cardiac death in dogs with pulmonic stenosis, with or without tricuspid regurgitation, that do not undergo balloon valvuloplasty or valve surgery. METHODS: Review of medical records of two UK referral centres between July 1997 and October 2008 for all cases of pulmonic stenosis that had no balloon valvuloplasty or valve surgery. Inclusion criteria included a diagnosis of pulmonic stenosis; spectral Doppler pulmonic velocity greater than 1·6 m/s; characteristic valve leaflet morphological abnormalities. Exclusion criteria included concurrent significant cardiac defects, including tricuspid dysplasia. Dogs with tricuspid regurgitation were included. Dogs were classified according to Doppler-derived pressure gradients into mild, moderate or severe pulmonic stenosis categories. RESULTS: Presence of tricuspid regurgitation and severe stenosis were independent predictors of cardiac death. A pulmonic pressure gradient of more than 60 mmHg was associated with 86% sensitivity, and 71% specificity of predicting cardiac death. CLINICAL SIGNIFICANCE: There is an increased probability of cardiac death in those cases which have a pulmonary pressure gradient greater than 60 mmHg and tricuspid regurgitation, though the effect of severity of tricuspid regurgitation on outcome was not measurable because of small sample sizes. These animals might benefit from intervention.

A retrospective study of 153 cases of undiagnosed collapse, syncope or exercise intolerance: the outcomes.

OBJECTIVES: To retrospectively assess the long-term outcome for dogs that were presented with collapse, syncope or exercise intolerance for which an underlying cause is not identified. METHODS: The clinical records of animals presenting to two practices were assessed. Dogs which presented for collapse, syncope or exercise intolerance at least 6 months previously and did not receive a definitive diagnosis despite investigation were included. Follow-up of these cases was carried out by conducting telephone interviews with the owners. RESULTS: One hundred and fifty-three cases were successfully followed up. Clinical signs had resolved in 64 cases (42%), 35 dogs (23%) were continuing to exhibit clinical signs, although 22 of these had improved without medical intervention. In 17 cases (11%), a diagnosis had subsequently been made or treatment was being administered and 37 dogs (24%) had died. Of the deaths, 18 (12%) were considered to be related to the original presentation. The overall prevalence of death and deterioration related to the problems investigated was 16·2% of cases. Death in boxers was significantly more common than in other breeds (36%). CLINICAL SIGNIFICANCE: Death and deterioration are uncommon outcomes for dogs other than boxers presenting with collapse, syncope and exercise intolerance for which a definitive diagnosis cannot be made.

Canine dilated cardiomyopathy: a retrospective study of prognostic findings in 367 clinical cases.

OBJECTIVE: To review the association between clinical signs and diagnostic findings and the survival time of dogs with dilated cardiomyopathy (DCM), and any influence of treatment prescribed. METHODS: A retrospective observational study of 367 dogs with DCM. Survival times until death or euthanasia for cardiac reasons were analysed using the Kaplan-Meier method plus univariate and multivariate Cox proportional hazards models. Two-tailed P values less than 0.05 were considered statistically significant. RESULTS: In the multivariate model, left ventricular diameter (LVDs)-index (P=0.0067), presence of pulmonary oedema on radiography (P=0.043), presence of ventricular premature complexes (VPCs) (P=0.0012), higher plasma creatinine (P=0.0002), lower plasma protein (P=0.029) and great Dane breed (P=0.0003) were negatively associated with survival. Most dogs were treated with angiotensin-converting enzyme inhibitors (93%) or furosemide (86%), and many received digoxin (50%) and/or pimobendan (30%). Thirteen dogs were lost to follow-up. No conclusions could be made in this study on the association between use of drugs and survival. CLINICAL SIGNIFICANCE: The LVDs-index was the single best variable for assessing the prognosis in this group of dogs with DCM. Other variables that were negatively associated with survival were presence of pulmonary oedema on radiography, presence of VPCs, higher plasma creatinine, lower plasma protein and great Dane breed.

Canine dilated cardiomyopathy: a retrospective study of signalment, presentation and clinical findings in 369 cases.

OBJECTIVE: To review the clinical and diagnostic findings and survival of dilated cardiomyopathy from a large population of dogs in England. METHODS: A retrospective study of the case records of dogs with dilated cardiomyopathy collected between January 1993 and May 2006. RESULTS: There were 369 dogs with dilated cardiomyopathy of which all were pure-bred dogs except for four. The most commonly affected breeds were dobermanns and boxers. Over 95 per cent of dogs weighed more than 15 kg and 73 per cent were male. The median duration of signs before referral was three weeks with 65 per cent presenting in stage 3 heart failure. The most common signs were breathlessness (67 per cent) and coughing (64 per cent). The majority of dogs (89 per cent) had an arrhythmia at presentation and 74 per cent of dogs had radiographic signs of pulmonary oedema or pleural effusion. The median survival time was 19 weeks. CLINICAL SIGNIFICANCE: Dilated cardiomyopathy occurs primarily in medium to large breed pure-bred dogs, and males are more frequently affected than females. The duration of clinical signs before referral is often short and the survival times are poor. Greater awareness of affected breeds, clinical signs and diagnostic findings may help in early recognition of this disease which often has a short clinical phase.

Transcatheter embolisation of patent ductus arteriosus using an Amplatzer vascular plug in six dogs.

OBJECTIVES: The objective of this study was to assess the feasibility of transcatheter embolisation of a patent ductus arteriosus using an Amplatzer vascular plug (Amplatzer Medical UK) in six dogs. METHODS: The Amplatzer vascular plug is a self-expandable, cylindrical device attached to a delivery cable. In all the dogs, the device was delivered transvenously. Successful device implantation was defined as firm anchorage of the device squarely within the distal part of the ductus arteriosus with no intra- or postoperative dislodgement. Successful occlusion of the ductus arteriosus occurred if a disappearance of the continuous murmur was achieved 24 hours after placement of the Amplatzer vascular plug. RESULTS: The age of the dogs ranged from 16 weeks to 7.5 years. Their weights ranged from 2.9 to 27.6 kg (median 6 kg). Two dogs had congestive heart failure before embolisation. Successful device implantation was achieved in all dogs. Successful occlusion of the ductus arteriosus was achieved in four of the six dogs. Complications included mild lameness, residual shunting, and bruising and pruritus around the surgical wound site. At follow-up, two dogs had a continuous murmur and one required treatment for congestive heart failure. CLINICAL SIGNIFICANCE: This technique may represent a clinically effective and less expensive alternative to the use of an Amplatzer duct occluder (Amplatzer Medical UK) in dogs with medium-sized patent ductus arteriosus. Further investigations are required to fully evaluate its efficacy and safety in various sizes and types of patent ductus arteriosus, and to determine the optimal device size in relation to the size of the ductus.

Results of pacemaker implantation in 104 dogs.

OBJECTIVES: To document the outcome, survival and complications involved in pacemaker implantation in dogs in a retrospective study. METHODS: Case records for all dogs in which pacemaker implantation was performed were reviewed. RESULTS: A total of 104 dogs underwent pacemaker implantation. Dogs were presented with atrioventricular (AV) block (71), sick sinus syndrome (25) or vasovagal syncope (eight). Age at presentation varied from six months to 13 years with a median age of seven years and two months. The Labrador was the most commonly represented breed (17 cases). All but one dog survived pacemaker implantation, with 93 showing resolution of their clinical signs while 10 dogs showed intermittent residual signs. One-, three- and five-year survival estimates were 86, 65 and 39 per cent, respectively. Major complications after implantation were documented in 15 dogs and three of these led to fatalities. Minor complications were noted in 23 dogs. Sudden death occurred in six dogs three to 55 months following successful pacemaker implantation. CLINICAL SIGNIFICANCE: Transvenous pacemaker implantation was successful in reducing or eliminating clinical signs in over 90 per cent of dogs with third-degree atrioventricular (AV) block or sick sinus syndrome. In dogs with vasovagal syncope, six of eight dogs had greatly reduced frequency of collapse and two became asymptomatic. Although the procedure was associated with complications, these were rarely life threatening and good survival was documented in the majority of cases.

Successful medical treatment of 15 dogs with pyothorax.

OBJECTIVES: To review the success of non-surgical management, which included antibiotics and a single thoracocentesis, in 15 dogs presenting with pyothorax. METHODS: Sixteen dogs were selected retrospectively from case files at the Veterinary Cardiorespiratory Centre. RESULTS: One dog was diagnosed with a mass suspected to be a pulmonary abscess on ultrasound examination and was referred for surgery. Fifteen dogs were treated medically. Springer spaniels were the most commonly presented breed (six cases) followed by Labrador retrievers (three cases). Under sedation or general anaesthesia, thoracocentesis was performed unilaterally and as much purulent effusion as possible was removed. Lavage of the thorax was not undertaken. In most dogs, antibiotic treatment was ampicillin at a mean dose of 33 mg/kg administered three times daily and 25 mg/kg metronidazole administered twice daily. Antibiotics were provided for a minimum of six weeks. All dogs recovered completely and did not show relapse on prolonged follow-up. This included one dog, which had very widespread pleural adhesions and minimal effusion. CLINICAL SIGNIFICANCE: In dogs that do not have evidence of pulmonary masses or consolidations and no evidence of granular pleural effusion, medical therapy may be curative even in chronic cases of pyothorax with pleural adhesions.

Idiopathic pericarditis in dogs: no evidence for an immune-mediated aetiology.

OBJECTIVE: To ascertain whether specific immunological changes are associated with canine pericardial effusion due to idiopathic pericarditis. METHODS: In this prospective study, serum antinuclear antibody and serum and pericardial fluid immunoglobulin (Ig) G, Ig M and Ig A concentrations were measured in dogs with pericardial effusion due to idiopathic pericarditis or pericardial neoplasia. The secretory index relative to albumin concentration was calculated in order to distinguish between Ig actively secreted into the pericardial fluid and that derived from the blood accumulating within the pericardial sac. Statistical analysis was performed comparing the results obtained between the two groups of dogs. RESULTS: Only three dogs were antinuclear antibody positive; two of these dogs had idiopathic pericarditis and one had neoplasia. Mean serum Ig M and Ig A concentrations were lower than the reference values in both groups, and the secretory indices for Ig M and Ig A were greater than 1.0. However, there was no significant difference with respect to any Ig measurement between the two groups of dogs (P>0.1). CLINICAL SIGNIFICANCE: The results of the present study do not support the hypothesis that canine idiopathic pericarditis has a significant 'immune-mediated' aetiology or immunological features that distinguish it from the pericardial changes associated with local neoplastic disease.

Treatment of congestive heart failure a neuroendocrine disorder.

The understanding of heart failure is no longer based on a supply and demand model of pump failure. Rather, heart failure is seen as a complex pathophysiological process with activation of various neuroendocrine systems. The goals of treatment have changed towards modifying these counterproductive neuroendocrine systems and slowing myocardial maladaptation. Angiotensin converting enzyme inhibitors are the only licensed drugs in veterinary practice that have a direct effect on neurohormones in heart failure. The range of drug options in human medicine is greater and some of these drugs are also increasingly being used in veterinary cardiology practice. This review describes the neuroendocrine systems involved in heart failure and discusses the range of drugs available in human and veterinary medicine. In doing so, it concentrates on the evidence available from good quality randomised trials in both the veterinary field and, where relevant, the human medical field.

Septic fibrinous pericarditis in a cocker spaniel.

A four-year-old cocker spaniel presented with cardiac tamponade due to a pericardial effusion, in addition to pyrexia and peripheral neutrophilia and a recent history of chest trauma. Cytological examination of the pericardial effusion revealed a predominant neutrophilia. The echocardiographic findings were of numerous hyperechoic densities in the pericardial space, due to fibrin, with concurrent thickening and distortion of the pericardium. Postmortem examination, including microbiology, revealed the presence of organising septic fibrinous pericarditis associated with a mixed infection of Streptococcus canis, Citrobacter species, Pseudomonas species and alpha-haemolytic streptococci.

Immunohistochemical characterisation of the lesions of canine idiopathic pericarditis.

Pericardial tissue was obtained from 14 dogs with idiopathic pericarditis, and from three dogs with pericardial effusion associated with neoplastic disease, for histopathological assessment and characterisation of infiltrating leucocytes by immunohistochemistry. The major pathological change was extensive pericardial fibrosis which was generally accompanied by a mixed inflammatory response that was of greatest intensity at the cardiac surface of the tissue. Perivascular lymphoplasmacytic aggregates were present at the pleural surface and within the fibrosed pericardium. There were no features that clearly distinguished the samples from dogs with neoplastic disease from dogs with idiopathic pericarditis. The pericardial infiltrates were dominated by MAC 387+ monocyte-macrophages and plasma cells expressing immunoglobulin (Ig)A or IgG. CD3+ T lymphocytes and major histocompatibility complex (MHC) class II+ macrophages were less common, although the perivascular aggregates were mixtures of T and B lymphocytes and a proportion of fibroblasts expressed MHC class II. There was no vascular pathology or deposition of immunoglobulin or complement within vessel walls. These findings are consistent with an immune response dominated by humoral effector mechanisms (Th2 immunity) but do not clearly support a primary immune-mediated pathogenesis for idiopathic pericarditis.