The variety of phenotypes behind 'double outlet right ventricle': clinical and imaging presentations in four dogs and a cat.

This report describes five cases of double outlet right ventricle (DORV) in four dogs (aged 3-18 months, two males and two females) and a domestic shorthair cat (aged 6 months, female) who presented with various clinical signs including tachypnea (n = 5), exercise intolerance (n = 5), mucous cyanosis (n = 3), delayed growth (n = 2), and/or lethargy (n = 2). The represented canine breeds were poodle, Yorkshire terrier, Samoyed, and Shetland sheepdog. For all animals, echocardiography revealed marked aortic dextroposition with both arterial trunks totally arising from the right ventricle, associated with a ventricular septal defect and various other congenital abnormalities, including subvalvular aortic stenosis (n = 2), minor aortic insufficiency (n = 5), subvalvular pulmonic stenosis with pulmonary trunk hypoplasia (n = 1), patent ductus arteriosus (n = 1), minor mitral and/or tricuspid dysplasia (n = 3). Subsequent cardiac remodeling was characterized by marked right ventricular hypertrophy for all patients, associated with right ventricular and right atrial dilation for most of them (4/5). Two dogs died soon after the initial DORV diagnosis (i.e. after 24 h and two months). A surgical correction attempted for another dog confirmed the presence of a DORV associated with patent ductus arteriosus, but the animal died during the procedure from sudden cardiac arrest. The fourth dog underwent a contrast-enhanced retrospective electrocardiogram-gated multidetector computed tomography angiography under general anesthesia, which confirmed the conotruncal malformation. Despite episodes of exercise intolerance, this dog is still alive, at the age of 53 months, as is the cat at the age of 21 months.

Atrial cardiomyopathy in an adult Labrador retriever dog.

INTRODUCTION: A 7-year-old castrated male Labrador retriever was examined for a 10-day history of weakness and syncope. Physical examination revealed bradycardia and a grade III/VI left apical systolic heart murmur. Electrocardiography demonstrated bradycardia, absence of P waves and an atrio-ventricular nodal escape rhythm. Echocardiography revealed marked biatrial enlargement. Thoracic radiographs showed no evidence of pulmonary edema. Routine plasma biochemistry and electrolytes, basal serum cortisol, total thyroxin concentration, and complete blood count were within normal limits. Serum cardiac troponin I concentration was moderately increased. Serological examinations for antibodies against vector-borne diseases were negative. A pacemaker was implanted one month after the initial presentation due to worsening of the dog's clinical condition despite medical treatment. The dog remained asymptomatic for 18 months but was then re-presented with a gastric dilatation volvulus and subsequently euthanized. Necropsy and histology of the heart yielded a diagnosis of atrial cardiomyopathy.

Antemortem diagnosis of a left auricular appendage herniation through a partial pericardial defect in a dog with degenerative mitral valve disease.

INTRODUCTION: A 14-year-old neutered male crossbreed dog was presented for weakness, cough and weight loss. Cardiac auscultation revealed tachycardia, arrhythmia and a grade V/VI left apical systolic heart murmur. Thoracic radiographs showed a large homogeneous soft tissue opacity in close contact with the cardiac silhouette in the left cranioventral mediastinum. Cardiac evaluation showed atrial fibrillation, degenerative mitral valve disease and a dilated left auricular appendage outside the pericardium consistent with herniation through a partial pericardial defect. Seven months after diagnosis, an atrial septal defect secondary to acquired atrial septal rupture was identified. The dog was euthanized thirteen months after initial presentation because of unresponsive clinical signs of congestive heart failure.

Systolic arterial blood pressure in small-breed dogs with degenerative mitral valve disease: a prospective study of 103 cases (2007-2012).

The objective of this prospective observational study was to assess systolic arterial blood pressure (SABP) in small-breed dogs with degenerative mitral valve disease (MVD) from different International Small Animal Cardiac Health Council (ISACHC) heart failure classes. For this purpose, 103 client-owned dogs weighing <20 kg (mean ± standard deviation, 8.5 ± 3.0 kg; aged 9.8 ± 2.9 years) and presenting with MVD diagnosed by echo-Doppler examination were enrolled. Nineteen healthy dogs (9.9 ± 2.3 years; 8.7 ± 4.2 kg) were concurrently recruited as controls. SABP was measured in unsedated dogs using the Doppler method according to the recommendations in the American College of Veterinary Medicine consensus statement. SABP was significantly increased in dogs in ISACHC class 1 (n=53; median, interquartile range 140 mmHg, 130-150 mmHg) and class 2 (n=21; 140 mmHg, 130-150 mmHg), compared to the control group (n=19; 130 mmHg, 120-140 mmHg; P<0.01 and P<0.05, respectively), but remained within the reference interval (≤ 160 mmHg). Conversely, dogs in ISACHC class 3 showed a significantly lower SABP (n=29, 120 mmHg, 110-130 mmHg) than those from all other ISACHC classes (P<0.001) and the controls (P<0.05). Additionally, SABP<120 mmHg was recorded in 13/103 dogs (13%). The 13 dogs were all ISACHC class 3 (3a or 3b) and were under medical treatment for heart failure. In conclusion, MVD was often associated with SABP values that were within the reference interval, but at its upper end. However, a significant decrease in SABP was observed in dogs with ISACHC heart failure class 3. Whether such low SABP values resulted from an MVD-related decrease in cardiac output, an afterload reduction owing to cardiac treatment, or both, remains to be determined.

Comparative echocardiographic and clinical features of hypertrophic cardiomyopathy in 5 breeds of cats: a retrospective analysis of 344 cases (2001-2011).

BACKGROUND: Primary hypertrophic cardiomyopathy (HCM) is the most common feline heart disease and has been demonstrated to be inherited in some breeds. However, few studies have compared HCM phenotypes and survival according to breed. OBJECTIVES: To compare epidemiological characteristics, clinical findings, left ventricular (LV) geometric patterns, and survival in several breeds of cats with HCM. ANIMALS: Three hundred and forty-four cats from 5 different breeds (Persian, Domestic Shorthair [DS], Sphynx, Maine coon [MC], and Chartreux) with primary HCM diagnosed by conventional echocardiography. METHODS: Retrospective study. Cats were classified according to breed and clinical status. RESULTS: Age at the time of diagnosis was lower (P < .001) in MC (median age, 2.5 years) and Sphynx (3.5 years) than in other breeds (OB), ie, 8.0, 8.0, and 11.0 years for DS, Chartreux, and Persians, respectively. The prevalence of LV outflow tract obstruction was higher (P < .001) in Persians (23/41; 56%) than in OB (115/303; 38%). Age at the first cardiac event was lower (P < .01) in MC (median age, 2.5 years) than in OB (7.0 years). All cats surviving > 15 years of age were DS, Persians, or Chartreux. Sudden death (representing 24% of all cardiac deaths) was observed only in 3 breeds (DS, MC, and Sphynx). CONCLUSION AND CLINICAL IMPORTANCE: As in humans, feline HCM is characterized by marked phenotypic variability with several breed-dependent features regarding epidemiology, LV geometric patterns, and clinical course (ie, age at diagnosis, 1st cardiac event, and cause of death).

Echocardiographic and tissue Doppler imaging alterations associated with spontaneous canine systemic hypertension.

BACKGROUND: Feline systemic arterial hypertension (SHT) is associated with a wide spectrum of left ventricular (LV) geometric patterns as well as diastolic, and to a lesser extent, systolic myocardial dysfunction. However, little is known about SHT-related cardiac changes in dogs. HYPOTHESIS: SHT in dogs is responsible for morphological and functional cardiac alterations. ANIMALS: Thirty dogs with spontaneous untreated SHT and 28 age- and body weight-matched healthy dogs as controls. METHODS: Prospective observational study. Conventional echocardiography and 2-dimensional color tissue Doppler imaging were performed in SHT dogs by trained observers and compared with controls. RESULTS: Forty-seven percent of SHT dogs (14/30) had diffuse concentric hypertrophy. None had left atrial dilatation and 10/30 (33%) had aortic insufficiency (AoI) associated with proximal aortic dilatation. Longitudinal diastolic left ventricular free wall (LVFW) motion was altered in all SHT dogs at the base (early to late diastolic wave ratio, E/A = 0.5 ± 0.1 versus 1.3 ± 0.3 for controls, P < .0001) and the apex (E/A = 1.6 ± 1.7 versus 3.9 ± 3.1, P < .05). Longitudinal motion of the interventricular septum at the base (E/A = 0.7 ± 0.4 versus 1.1 ± 0.1, P < .01) and radial LVFW motion in the subendocardium (E/A = 0.9 ± 0.5 versus 1.6 ± 0.3, P < .01) were also altered in dogs with SHT. Longitudinal LVFW systolic velocities and gradients were also significantly decreased (P < .05) in SHT dogs. CONCLUSION AND CLINICAL IMPORTANCE: As in SHT in cats, SHT in dogs is associated with myocardial dysfunction independently of the presence of myocardial hypertrophy. However, unlike feline SHT, it results in a homogeneous LV geometric pattern with a relatively high prevalence of AoI.