Effect of dietary canola oil on long‐chain omega‐3 fatty acid content in broiler hearts

Young and healthy broilers are susceptible to sudden death syndrome (SDS), which is caused by cardiac arrhythmia. The long‐chain ‘fish‐type’ omega‐3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have cardioprotective anti‐arrhythmic effects in animals and humans. Raising the cardiac level of EPA and DHA in chickens may protect against SDS. However, fish oil as a source of EPA and DHA in poultry feed is costly and introduces undesirable properties to the meat. Whilst omega‐3 vegetable oils, such as canola oil, are cheaper and do not have a strong odour, they contain the short‐chain fatty acid α‐linolenic acid, which requires conversion to EPA and DHA after ingestion. We investigated the capacity for dietary canola oil to elevate cardiac EPA and DHA in broilers. Broilers were fed with diets containing either 3% canola oil or tallow, which is currently used in some commercial feeds. Upon completion of a 42 day feeding trial, canola oil significantly increased EPA and EPA + DHA in heart phospholipids relative to tallow. The elevation in cardiac EPA and EPA + DHA may provide anti‐arrhythmic effects and protect against SDS in poultry. This proof‐of‐concept biochemical study suggests that a larger study to assess the clinical outcome of SDS may be warranted.     

Fibrinous pericarditis and cardiac tamponade in a 3‐week‐old pony foal

A 3‐week‐old Pony of the Americas foal presented with a history of respiratory distress presumed to result from Actinobacillus equuli pleuropneumonia and septic arthritis. Failure of transfer of passive colostral immunity was suspected, but not confirmed, based on a history of the foal being separated from its dam shortly after parturition. Transient improvement was noted following thoracocentesis and removal of approximately 600 ml of pleural fluid but progressive clinical signs of congestive heart failure developed. Fibrinous pericarditis with evidence of cardiac tamponade was subsequently diagnosed via thoracic ultrasonography. Early clinical signs of cardiogenic shock were identified and fibrinopurulent exudate removed through a catheter placed with ultrasound guidance into the pericardium. The foal experienced cardiorespiratory arrest during the procedure and died despite resuscitative efforts. Post mortem examination identified extensive hypertrophy of the pericardium, septic arthritis, mild pleural effusion and focal bronchopneumonia. This report details the clinical evaluation, haematology, treatment and post mortem pathology of a foal with Actinobacillus equuli associated fibrinous pericarditis, as well as a brief review of cardiac tamponade.     

牛心型α肌动蛋白基因的进化及表达研究

试验旨在对鲁西黄牛心型α肌动蛋白的进化及表达进行研究,为研究该基因的功能提供依据。试验采用生物信息学方法对心型α肌动蛋白的进化进行了分析,利用Western blotting和免疫荧光的方法分析了牛心型α肌动蛋白的表达模式。结果显示,心型α肌动蛋白除在鲁西黄牛心脏组织中有强表达外,在骨骼肌中也检测到该蛋白的表达。推测心型α肌动蛋白除在成体鲁西黄牛的心脏发育过程中起作用外,在骨骼肌发育过程中也起作用。     

Reversed patent ductus arteriosus and multiple congenital malformations in an 8‐day‐old Arabo‐Friesian foal

An 8‐day‐old Arabo‐Friesian filly was presented with signs of severe dyspnoea, tachypnoea, coughing and cyanotic mucous membranes. On auscultation, a bilateral grade V/VI continuous heart murmur and heart rate of 155 beats/min (sinus tachycardia) were detected. Lung ultrasonography revealed pronounced comet tail artefacts indicating lung oedema. Echocardiography showed right ventricular hypertrophy, a 1.2 cm muscular ventricular septal defect with a left‐to‐right shunt, a stenotic bicuspid pulmonary valve and severe mitral and tricuspid valve regurgitation. Tricuspid regurgitation peak velocity indicated a right ventricular systolic pressure of 119 mmHg. The pulmonary artery was severely dilated and a 1 cm diameter patent ductus arteriosus was found. Colour flow Doppler showed systolic ductal flow reversal with right‐to‐left shunting through the ductus. Arterial partial oxygen pressure and saturation were lower in the metatarsal artery (25 mmHg, saturation 52.6%) than in the carotid artery (31 mmHg, saturation 64.3%). Due to the poor prognosis, the foal was subjected to euthanasia and necropsy confirmed the ultrasonographic findings. Patent ductus arteriosus is a rare condition and occurs most frequently in combination with tetralogy and pentalogy of Fallot. A genetic basis for congenital cardiac disease, especially for ventricular septal defects, in Arabians and for aortic rupture and aorto‐pulmonary fistulation in Friesians has been reported. Whether cross‐breeding leads to an increased prevalence is unknown. This is the first case report with echocardiographic visualisation of reversed ductal flow in a neonatal Arabo‐Friesian foal.     

64‐MULTIDETECTOR COMPUTED TOMOGRAPHIC ANGIOGRAPHY OF THE CANINE CORONARY ARTERIES

Canine coronary artery angiography (CTA) was performed in four anesthetized healthy dogs using 64‐multidetector computed tomography. Esmolol, a β‐1 adrenergic receptor antagonist, and sodium nitroprusside, an arteriolar and venous dilator, were administered to enhance visualization of the coronary arteries by reducing heart rate and creating vasodilation. The left main coronary artery with its three main branches and the right coronary artery were visualized and subdivided in 13 segments for evaluation. Optimal reconstruction interval, expressed as percentage of the R‐to‐R interval, was determined at 5% in 2.9%, 35% in 1%, 75% in 21.2%, 85% in 43.3%, and 95% in 31.7% of the segments. Overall image quality was good in 41.3% of the segments and excellent in 14.4%. There was blur in 98.1%, motion in 17.3%, and stair step in 6.7% of the evaluated segments, but these artifacts did not interfere with anatomic depiction of the arteries. Cross‐sectional anatomy of the coronary arteries as evaluated from the coronary CTA agreed well with gross anatomic evaluation and published information. The use of esmolol did not lead to the target heart rate of 60–65 beats/min. Nitroprusside had no significant effect on visualized length or diameter of the coronary artery branches. Coronary CTA is useful for the anatomic depiction of coronary artery branches in the dog.     

The renin‐angiotensin‐aldosterone system and its suppression

Chronic activation of the renin‐angiotensin‐aldosterone system (RAAS) promotes and perpetuates the syndromes of congestive heart failure, systemic hypertension, and chronic kidney disease. Excessive circulating and tissue angiotensin II (AngII) and aldosterone levels lead to a pro‐fibrotic, ‐inflammatory, and ‐hypertrophic milieu that causes remodeling and dysfunction in cardiovascular and renal tissues. Understanding of the role of the RAAS in this abnormal pathologic remodeling has grown over the past few decades and numerous medical therapies aimed at suppressing the RAAS have been developed. Despite this, morbidity from these diseases remains high. Continued investigation into the complexities of the RAAS should help clinicians modulate (suppress or enhance) components of this system and improve quality of life and survival. This review focuses on updates in our understanding of the RAAS and the pathophysiology of AngII and aldosterone excess, reviewing what is known about its suppression in cardiovascular and renal diseases, especially in the cat and dog.     

Elimination half‐life of intravenously administered equine cardiac troponin I in healthy ponies

Reasons for performing study: To date, no information is available on the true biological elimination half‐life (T_1/2) of cardiac troponin I (cTnI) in the equine species. Such data are required to better evaluate the optimal time to acquire the cTnI sample following acute myocardial injury. Objective: To determine the T_1/2 of equine cTnI. Methods: Four healthy ponies received i.v. injections of recombinant equine cTnI. Plasma cTnI concentrations were measured with a point‐of‐care cTnI analyser at multiple time points after injection. Standard pharmacokinetic analysis was performed to establish the T_1/2 of cTnI. Results: The average T_1/2 of cTnI was determined to be 0.47 h using a single rate elimination model. Conclusion: The elimination of recombinant equine cTnI following i.v. administration is very rapid. Establishing the T_1/2 of troponin provides critical information in understanding the clinical application of this cardiac biomarker in equine practice.     

The clinical practice of CPCR in small animals: an internet‐based survey

Objective – To characterize the provision of CPCR by small animal veterinarians in clinical practice and to assess how this practice varies among different levels of expertise. Design – Internet‐based survey. Setting – Academia, referral practice, and general practice. Subjects – Six hundred and two small animal veterinarians in clinical practice. Respondents were grouped a priori according to level of expertise: board‐certified (ACVECC, ACVA, ECVAA) specialists; general practitioners in emergency clinics; general practitioners in general practice (GPG). Interventions – Email invitations to the online questionnaire were disseminated via a veterinary internet platform and mailing list server discussion groups. Questions explored respondent characteristics, CPCR preparedness, infrastructural and personnel resources, and techniques of basic and advanced life support. Main Results – In this group of practitioners, the majority (65%) were in general practice. GPG were more likely to perform CPCR <5 times per year and to have 3 or fewer members on their resuscitation team. Most practitioners have a crash cart and drug‐dosing chart available. GPG were less likely to obtain resuscitation codes on their patients, and less likely to use end‐tidal carbon dioxide monitoring or defibrillation. Intubation, oxygen supplementation, vascular access, and external thoracic compressions were widely used, however, GPG were more likely to use lower chest compression rates. Drugs used for CPCR differed among the groups with GPG more likely to use doxapram and glucocorticoids. Conclusions – CPCR is heterogeneously performed in small animal veterinary medicine; differences exist, both among and within different types of veterinarians with varying levels of expertise, in respect to available infrastructure, personnel and CPCR techniques used.     

An exploratory investigation of echocardiographic parameters and the effects of posture on cardiac structure and function in the Livingstone's fruit bat (Pteropus livingstonii)

There is growing evidence that dilated cardiomyopathy may be a major cause of death in captive Livingstone's fruit bats (Pteropus livingstonii). Therefore, the primary aim of this prospective, exploratory study was to examine whether a systematic cardiac ultrasound protocol is feasible in this critically endangered species and to report basic measures of cardiac structure and function from a cohort of apparently healthy bats. A secondary aim was to test the effect posture (dorsal recumbency vs. roosting) has upon cardiac function in this species. Transthoracic echocardiograms, including 2D, Doppler, and tissue Doppler measures of cardiac structure and function were completed as part of routine health examinations for bats at a single center (n = 19). Bats were then grouped by age and disease status and the mean and range data reported for each group. In healthy adult bats, with the exception of a reduction in heart rate (P ≤ 0.05), right atrial systolic area (P ≤ 0.05), and right ventricular velocity during atrial contraction, there were no significant changes in cardiac structure or function in response to the roosting position. However, in the bats presenting with dilated cardiomyopathy the current data suggest that left ventricular ejection fraction is improved while roosting. Further work is required to confirm our initial findings, generate diagnostic reference intervals, and explore the causes of dilated cardiomyopathy in this species.     

Assessment of a point‐of‐care cardiac troponin I test to differentiate cardiac from noncardiac causes of respiratory distress in dogs

Objectives – To (1) determine a reference interval for cardiac troponin I (cTnI) using a point‐of‐care device in normal dogs and compare the results with those published by the manufacturer and (2) determine if cTnI differs among dogs with cardiogenic and noncardiogenic respiratory distress. Design – Prospective observational study. Setting – Emergency and referral veterinary hospital. Animals – Twenty‐six clinically normal dogs and 67 dogs in respiratory distress. Interventions – All dogs underwent whole blood sampling for cTnI concentrations. Measurements and Results – Normal dogs had a median cTnI concentration of 0.03 ng/mL (range 0–0.11 ng/mL). Thirty‐six dogs were diagnosed with noncardiogenic respiratory distress with a median cTnI concentration of 0.14 ng/mL (range 0.01–4.31 ng/mL). Thirty‐one dogs were diagnosed with cardiogenic respiratory distress with a median cTnI concentration of 1.74 ng/mL (range 0.05–17.1 ng/mL). A significant difference between cTnI concentrations in normal dogs and dogs with noncardiogenic respiratory distress was not detected. Significant differences in cTnI concentrations were found between normals versus cardiogenic and cardiogenic versus noncardiogenic respiratory distress groups. Significant differences in cTnI concentrations were identified in >10 when compared with the <5 and the 5–10 years of age groups. Receiver operating curve analysis identified cTnI concentrations >1.5 ng/mL as the optimal “cut‐off point” having a sensitivity of 78% and specificity of 51.5%. The area under the receiver operating curve was 0.72. Overall test accuracy was 65%. Conclusions – cTnI concentrations were significantly increased in dogs with cardiogenic respiratory distress versus dogs with noncardiogenic respiratory distress and normal dogs. A significant difference between normal dogs and dogs with noncardiogenic causes of respiratory distress was detected. Although highly sensitive when cTnI concentrations exceed 1.5 ng/mL, the test has low specificity. Assessment of cTnI by the methodology used cannot be recommended as the sole diagnostic modality for evaluating the cause of respiratory distress in dogs.     

Mitral valve and tricuspid valve dysplasia in a 9‐week‐old Standardbred colt

A 9‐week‐old Standardbred colt was presented for investigation of dull demeanour, exercise intolerance and heart murmurs. Cardiac auscultation revealed a grade 5/6 holosystolic murmur and a grade 5/6 pansystolic murmur over the left and right cardiac apex respectively, and an irregularly irregular cardiac rhythm. Electrocardiographic examination findings were consistent with atrial fibrillation and tachycardia. Echocardiographic examination identified marked atrioventricular regurgitation and atrial dilation bilaterally, thickening of the mitral and tricuspid valves and dilation of the pulmonary artery consistent with pulmonary hypertension. No ventricular or atrial septal defect was present. Cardiomegaly and diffuse pulmonary oedema were evident on examination of lateral thoracic radiographs. Dysplasia of the mitral and tricuspid valves, eccentric cardiomegaly and pulmonary oedema were confirmed by post mortem examination. Dysplasia of the atrioventricular valves represents a rare cause of biventricular failure in the horse.