Clinical presentation, management, and survival in dogs with persistent atrial standstill in the United Kingdom.

OBJECTIVES: To investigate the clinical and echocardiographic presentation of dogs with persistent atrial standstill (PAS), identify variables measured at first presentation that could predict their survival, and document the progression of the disease after pacing. MATERIALS AND METHODS: Retrospective study of medical records of dogs diagnosed with PAS at three referral hospitals of the United Kingdom over seven years. RESULTS: Twenty-six dogs were diagnosed with PAS during the study period. Median age of the population was three years (range: seven months-12.5 years). The most common clinical sign was syncope (14/26). Twenty-four dogs received artificial pacemakers (PM). Major complications after PM implantation were observed in four dogs (four/24). Serial echocardiographic examinations showed that cardiac dimensions of PAS dogs with left atrial or left ventricular dilation at first presentation did not return to reference range after pacing. Further dilation of the cardiac chambers, recurrence of congestive heart failure (CHF), or development of new episodes of CHF were documented in seven, four, and 10 PAS dogs, respectively, despite pacing. Median survival time for cardiac-related deaths after PM implantation was 1512 days (18-3207). Neither CHF nor echocardiographic variables at presentation predicted survival after PM implantation in PAS dogs. CONCLUSIONS: Persistent atrial standstill (PAS) is an uncommon bradyarrhythmia, occurring in young adult dogs. Affected dogs were often presented with syncope. Whilst syncope resolved, cardiac remodeling persisted after PM implantation. Long-term survival was favorable after PM implantation and was not predicted by congestive status or cardiac chamber size at first presentation.

Pacemaker-lead-associated thrombosis in dogs: a multicenter retrospective study.

INTRODUCTION: Pacemaker implantation is the treatment of choice for clinically relevant bradyarrhythmias. Pacemaker-lead-associated thrombosis (PLAT) occurs in 23.0-45.0% of people with permanent transvenous pacemakers. Serious thromboembolic complications are reported in 0.6-3.5%. The incidence of PLAT in dogs is unknown. ANIMALS, MATERIALS AND METHODS: multicenter retrospective study of seven centers with 606 client-owned dogs undergoing permanent pacemaker implantation between 2012 and 2019. 260 dogs with a transvenous pacemaker with echocardiographic follow-up, 268 dogs with a transvenous pacemaker without echocardiographic follow-up and 78 dogs with an epicardial pacemaker. RESULTS: 10.4% (27/260) of dogs with transvenous pacemakers and echocardiographic follow-up had PLAT identified. The median time to diagnosis was 175 days (6-1853 days). Pacemaker-lead-associated thrombosis was an incidental finding in 15/27 (55.6%) dogs. Of dogs with a urine protein:creatinine ratio measured at pacemaker implantation, dogs with PLAT were more likely to have proteinuria at pacemaker implantation vs. dogs without PLAT (6/6 (100.0%) vs. 21/52 (40.4%), P=0.007). Urine protein:creatinine ratio was measured in 12/27 (44.4%) dogs at PLAT diagnosis, with proteinuria identified in 10/12 (83.3%) dogs. Anti-thrombotic drugs were used following the identification of PLAT in 22/27 (81.5%) dogs. The thrombus resolved in 9/15 (60.0%) dogs in which follow-up echocardiography was performed. Dogs with PLAT had shorter survival times from implantation compared to those without PLAT (677 days [9-1988 days] vs. 1105 days [1-2661 days], P=0.003). CONCLUSIONS: Pacemaker-lead-associated thrombosis is identified in 10.4% (27/260) of dogs following transvenous pacing, is associated with proteinuria, can cause significant morbidity, and is associated with reduced survival times.

Analysis of canine cardiovascular therapeutic agent prescriptions using electronic health records in primary care veterinary practices in the United Kingdom.

INTRODUCTION/OBJECTIVES: Canine cardiovascular (CV) diseases are often managed in primary care settings. The objectives were to describe CV therapeutic agent (CVTA) prescribing patterns in primary care practices in the United Kingdom (UK) and to evaluate recorded clinical signs, diagnostic tests and justifications for use of torasemide, a recently marketed and authorised loop-diuretic in the UK. ANIMALS, MATERIALS AND METHODS: Electronic health records (EHRs) describing 3,579,420 consultations (1,043,042 unique dogs) were collated (1 April 2014 and 31 December 2018) by the Small Animal Veterinary Surveillance Network from 270 veterinary practices. Consultations prescribing at least one CVTA were identified. Annual variation in individual CVTA prescriptions was analysed using mixed-effects binomial regression models. Free-text clinical narratives were manually read to determine the first-prescribing event for torasemide. RESULTS: Twenty-nine thousand and seven consultations (0.81% of all consultations, 95% confidence interval [CI], 0.76-0.86) prescribed CVTA in 14,148 (1.36%) dogs. Furosemide (52.8% of CV-prescribing consultations, 95% CI 50.7-54.9) and pimobendan (51.9%, 95% CI 50.1-53.7) were most prescribed. Longitudinal analysis (2014-2018) showed a significant negative temporal trend for angiotensin-converting enzyme inhibitors (p < 0.001), and furosemide (p = 0.003) and a positive temporal trend for pimobendan (p = 0.020) and torasemide (p < 0.001). First prescriptions of torasemide were identified in 16.5% of torasemide-prescribing consultations. Where justification for prescription of torasemide was identified (32.5%), furosemide resistance was the most common (92.0%). CONCLUSIONS: EHRs can be used to temporally monitor prescribing habits, including responses to market authorisations. Despite authorisation in the UK for torasemide use as a first-line diuretic, it was most commonly prescribed after furosemide resistance.

Clinical and diagnostic imaging findings in dogs with atrial appendage aneurysm: 7 cases (2014-2020).

INTRODUCTION/OBJECTIVE: Atrial appendage aneurysm in dogs is a rare condition and has not been well described. The aim of this study is to describe clinical and diagnostic imaging findings, especially computed tomography (CT), of atrial appendage aneurysms in dogs. ANIMALS: Seven client-owned dogs with a presumptive diagnosis of left or right atrial appendage aneurysm. MATERIALS AND METHODS: Retrospective study. Medical records were searched to identify dogs with a presumptive diagnosis of left (LAAA) or right atrial appendage aneurysm (RAAA). Signalment, history, examination findings, diagnostic test results, and imaging procedures were reviewed. Archived diagnostic images were retrieved and evaluated by two board-certified radiologists and a board-certified cardiologist. Data analysis was descriptive. RESULTS: Six cases were diagnosed with RAAA and one with LAAA with a median age of 8 years. Five affected dogs were small to medium-breed male dogs. All dogs underwent a thoracic CT examination for various reasons and all cases of RAAA were incidental findings. CT was useful to identify and assess the atrial appendage aneurysm, as well as neighboring structures, although possible pericardial defects could not be visualized. Five dogs had a concurrent echocardiographic examination, which successfully identified the LAAA and two RAAA. CONCLUSIONS: This case series described the clinical and CT findings in seven dogs with atrial appendage aneurysm, as well as echocardiographic findings in five of these cases. Right atrial appendage aneurysms appear to be mainly incidental findings. CT seems to be more sensitive than echocardiography in the detection of atrial appendage aneurysm.

Glucocorticoid metabolism and the action of 11 beta-hydroxysteroid dehydrogenase 2 in canine congestive heart failure.

The enzyme 11-beta-hydroxysteroid dehydrogenase isoenzyme 2 (11BHSD2) is responsible for converting the active glucocorticoid cortisol to inactive cortisone and in the renal medulla protects the mineralocorticoid receptor (MR) from activation by cortisol. Derangements in 11BHSD2 activity can result in reduced conversion of cortisol to cortisone, activation of the MR by cortisol and, consequently, sodium and water retention. The objective of this study was to examine glucocorticoid metabolism in canine congestive heart failure (CHF), specifically to evaluate whether renal 11BHSD2 activity and expression were altered. Dogs were prospectively recruited into one of two phases; the first phase (n=56) utilized gas chromatography-tandem mass spectrometry to examine steroid hormone metabolites normalised to creatinine in home-caught urine samples. Total serum cortisol was also evaluated. The second phase consisted of dogs (n=18) euthanased for refractory CHF or for behavioural reasons. Tissue was collected from the renal medulla for examination by quantitative reverse transcription polymerase chain reaction, immunohistochemistry and protein immune-blotting. Heart failure did not change urinary cortisol:cortisone ratio (P=0.388), or modify renal expression (P=0.303), translation (P=0.427) or distribution of 11BHSD2 (P=0.325). However, CHF did increase excretion of 5α-tetrahydrocortisone (P=0.004), α-cortol (P=0.002) and α-cortolone (P=0.009). Congestive heart failure modifies glucocorticoid metabolism in dogs by increasing 5α-reductase and 20α-hydroxysteroid dehydrogenase activity. Differences between groups in age, sex and underlying disease processes may have influenced these results. However, 11BHSD2 does not appear to be a potential therapeutic target in canine CHF.

Total anomalous pulmonary venous connection in a mature dog.

A 2-year 10-month, male neutered, crossbreed dog presented for evaluation of cyanosis and exercise intolerance. Doppler echocardiography revealed severe dilation of the right atrium and right ventricle with moderate pulmonary hypertension. Right-to-left shunting across a large ostium secundum atrial septal defect was confirmed by contrast echocardiography. Thoracic radiography revealed a vascular pattern together with cardiomegaly. Computed tomography angiography identified an anomalous pulmonary venous connection in which all pulmonary veins, apart from the right middle vein, coalesced into a single, large aneurysmal vein that then drained into the right atrium via the cranial vena cava. The distal opening of the right middle pulmonary vein could not be determined. A presumptive diagnosis of partial anomalous pulmonary venous connection was made. The dog was medically managed with sildenafil (1.5 mg/kg by mouth [PO] every 8 h) and remained clinically stable for 2 months before euthanasia due to worsening exercise intolerance. On postmortem examination, all pulmonary veins, including the right middle vein, were shown to communicate with a single, large central vein. This large vein then connected with the right atrium via the cranial vena cava, consistent with a total anomalous pulmonary venous connection. This case report describes a rare congenital abnormality which has not been previously reported in a mature dog.

Changes of SERCA activity have only modest effects on sarcoplasmic reticulum Ca2+ content in rat ventricular myocytes.

Changes of the activity of the sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA) affect the amplitude of the systolic Ca(2+) transient and thence cardiac contractility. This is thought to be due to alterations of SR Ca(2+) content. Recent work on mice in which the expression of SERCA is decreased found that a large reduction of SERCA expression resulted in a proportionately much smaller decrease of SR Ca(2+) content. The aim of the current work was to investigate the quantitative nature of the dependence of both the amplitude of the systolic Ca(2+) transient and SR Ca(2+) content on SERCA activity during acute partial inhibition of SERCA. Experiments were performed on rat ventricular myocytes. Brief application of thapsigargin (1 µm) resulted in a decrease of SERCA activity as measured from the rate of decay of the systolic Ca(2+) transient. This was accompanied by a decrease in the amplitude of the systolic Ca(2+) transient which was linearly related to that of SERCA activity. However, the fractional decrease in the SR Ca(2+) content was much less than that of SERCA activity. On average SR Ca(2+) content was proportional to SERCA activity raised to the 0.38 ± 0.07 power. This shallow dependence of SR content on SERCA activity arises because Ca(2+) release is a steep function of SR Ca(2+) content. In contrast SR Ca(2+) content was increased 4.59 ± 0.40 (n = 8)-fold by decreasing ryanodine receptor opening with tetracaine (1 mm). Therefore a modest decrease of SR Ca(2+) content results in a proportionately larger fall of Ca(2+) release from the SR which can balance a larger initiating decrease of SERCA. In conclusion, the shallow dependence of SR Ca(2+) content on SERCA activity is expected for a system in which small changes of SR Ca(2+) content produce larger effects on the amplitude of the systolic Ca(2+) transient.