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OBJECTIVES : To determine the underlying disease prevalence in acute feline dyspnoea and to examine whether historical and clinical examination findings can differentiate between acute cardiac and noncardiac dyspnoea in cats in primary practice. MATERIALS AND METHODS :We prospectively enrolled cats presenting with dyspnoea for the first time to primary practice between June 1, 2011 and October 31, 2016. We collected signalment, historical and clinical data at presentation using a standard form. Cases were investigated by primary clinicians, and the final diagnosis was confirmed by the authors. Records lacking critical data were excluded.Relationships between historical or clinical variables and dyspnoea aetiology were examined. Diagnostic test performance analyses were used to find optimal cut-off values for select historical or clinical variables that could differentiate cardiac and non-cardiac dyspnoea.RESULTS : Participants included 108 cats. A definitive diagnosis was reached in 92 cases; 60 were cardiac (65%), 15 respiratory (16%), 10 neoplastic (11%) and 7 traumatic (8%). Of cats with cardiac dyspnoea, 25% had a history of cough. A gallop sound, rectal temperature less than 37·5°C, heart rate of greater than 200 bpm and respiratory rate greater than 80 per minute were all useful to predict cardiac-associated dyspnoea. A triage algorithm using these findings in combination was designed to optimise the rapid diagnosis of probable cardiac dyspnoea.

Aims Subclinical left ventricular dysfunction (LVD) is a prelude to symptomatic heart failure (HF). We hypothesised that screening‐guided treatment with spironolactone would prevent incident HF in at‐risk patients. Methods and results We randomised asymptomatic, community‐dwelling subjects aged ≥65 years old, with at least one non‐ischaemic HF risk factor (hypertension, type 2 diabetes mellitus or obesity) to echocardiography‐guided therapy or usual care. Spironolactone therapy was triggered by the detection of subclinical LVD (global longitudinal strain [GLS] ≤16%) or diastolic abnormalities (at least one of E/e′ >15, E/e′ >10 with left atrial enlargement [LAE] or impaired relaxation [E/A < 0.8, IR], LAE with IR), or borderline GLS (17%) with IR or borderline GLS with LAE. The primary outcome was incident HF at 24 months. Secondary outcomes were change in 6‐min walk test (6MWT) and change in left ventricular function. LVD was identified in 161 (46%) of 349 participants (age 70 [68–73] years, 201 [58%] women). The trial was stopped because of a 55% rate of spironolactone discontinuation, due primarily to decline in renal function. Incident HF developed in 11 (3.5%) of 310 participants completing follow‐up, with no difference between usual care and intervention (4 [2.5%] vs. 7 [4.7%], p = 0.29), decline in 6MWT distance (p = 0.28), persistent or new LVD (p = 0.58), nor change in GLS with intervention (p = 0.15). A per‐protocol analysis of 131 patients with baseline LVD and a follow‐up echocardiogram, showed resolution of LVD with spironolactone therapy (59% vs. 33%, p = 0.01). Conclusion The study was underpowered to determine whether screening‐guided spironolactone therapy reduced incident HF because spironolactone was frequently discontinued due to renal function criteria. However, LVD resolved in more patients treated with spironolactone than in untreated patients. Future trials should use less conservative renal criteria for spironolactone discontinuation.

Background Envenomation by the European adder ( Vipera berus ) is common in dogs in Europe. Cardiac arrhythmias occur but clinical studies of envenomated dogs are limited. Objectives To describe arrhythmias in dogs within 48 hours of envenomation, and investigate associations between arrhythmia grade, serum troponin I (cTnI), and snakebite severity score (SS score). Animals Twenty‐one client‐owned dogs bitten by V berus . Methods Prospective cohort study of envenomated dogs. Ambulatory electrocardiograms were recorded from presentation to 48 hours after snakebite, and arrhythmias graded 0 to 3 based on frequency and severity. Serum cTnI was measured at presentation, 12 hours, 24 hours, 36 hours, and 14 days after bite. An SS score of 1 to 3 was recorded at admission and based on clinical examination. Results All dogs survived. Twelve dogs (57%) developed arrhythmias, all of which were ventricular in origin. Severe complex ventricular arrhythmias (VAs) were observed in 6 dogs (29%). Eighty‐one percent of dogs (n = 17) had increased cTnI concentrations at 1 or more time points. Dogs that developed arrhythmias had significantly higher concentrations of cTnI at 12 hours (1.67 [0.04‐32.68] versus 0.03 [0.01‐0.052]; P = .002), 24 hours (1.88 [0.2‐14.23] versus 0.06 [0.01‐2.06]; P = .009), and 36 hours (3.7 [0.02‐16.62] versus 0.06 [0.01‐1.33]; P = .006) after bite compared to those that did not. Contingency table analysis showed that SS score was not significantly associated with arrhythmia grade ( P = .9). Conclusions and Clinical Importance Myocardial cell injury, reflected by increased cTnI concentrations and VAs, is common after V berus envenomation in dogs. Prolonged electrocardiography monitoring is advised, particularly where cTnI is increased.

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