Cardiac tumours are uncommon in the canine and feline population and often an incidental finding. Common types include haemangiosarcoma (HSA), aortic body tumours (chemodectoma and paraganglioma) and lymphoma. These neoplasms can cause mild to severe, life-threatening clinical signs that are independent of the histological type and may be related to altered cardiovascular function or local haemorrhage/effusion into the pericardial space. Cardiac tumours may require symptomatic treatment aimed at controlling tumour bleeding and potential arrhythmias, and other signs caused by the mass effect. Additional treatment options include surgery, chemotherapy and radiotherapy. For all medical therapies, complete remission is unlikely and medical management, beyond adjunctive chemotherapy in HSA, requires further investigation but combination chemotherapy is recommended for lymphoma. The aim of this report is to summarize and critically appraise the current literature in a descriptive review. However, interpretation is limited by the lack of definitive diagnosis and retrospective nature of most studies.
BackgroundAtrial fibrillation (AF) usually is associated with a rapid ventricular rate. The optimal heart rate (HR) during AF is unknown.Hypothesis/ObjectivesHeart rate affects survival in dogs with chronic AF.AnimalsForty‐six dogs with AF and 24‐hour ambulatory recordings were evaluated.MethodsRetrospective study. Holter‐derived HR variables were analyzed as follows: mean HR (meanHR, 24‐hour average), minimum HR (minHR, 1‐minute average), maximum HR (maxHR, 1‐minute average). Survival times were recorded from the time of presumed adequate rate control. The primary endpoint was all‐cause mortality. Cox proportional hazards analysis identified variables independently associated with survival; Kaplan‐Meier survival analysis estimated the median survival time of dogs with meanHR <125 bpm versus ≥125 bpm.ResultsAll 46 dogs had structural heart disease; 31 of 46 had congestive heart failure (CHF), 44 of 46 received antiarrhythmic drugs. Of 15 dogs with cardiac death, 14 had CHF. Median time to all‐cause death was 524 days (Interquartile range (IQR), 76–1,037 days). MeanHR was 125 bpm (range, 62–203 bpm), minHR was 82 bpm (range, 37–163 bpm), maxHR was 217 bpm (range, 126–307 bpm). These were significantly correlated with all‐cause and cardiac‐related mortality. For every 10 bpm increase in meanHR, the risk of all‐cause mortality increased by 35% (hazard ratio, 1.35; 95% CI, 1.17–1.55; P < 0.001). Median survival time of dogs with meanHR<125 bpm (n = 23) was significantly longer (1,037 days; range, 524‐open) than meanHR ≥125 bpm (n = 23; 105 days; range, 67–267 days; P = 0.0012). Mean HR was independently associated with all‐cause and cardiovascular mortality (P < 0.003).Conclusions and Clinical ImportanceHolter‐derived meanHR affects survival in dogs with AF. Dogs with meanHR <125 bpm lived longer than those with meanHR ≥ 125 bpm.
Serial Doppler echocardiographic examinations were carried out in random order on six boxer dogs, on 3 separate days, by two experienced Doppler echocardiographers, to assess measurement variability and reproducibility of 65 parameters. Large numbers of parameters exhibited significant differences for each of the categories of intraobserver, interobserver, interday and interoperator. The coefficients of variation for all parameters measured ranged from 5.03 to 46.43%, but most were less than 20%. In general, least variation was found for the intraobserver category, and the best reproducibility for M-mode and left ventricular volumetric data. The worst reproducibility was found for tricuspid inflow and pulmonary venous flow measurements. The results of this study suggest differences greater than 20% for serial scans must be achieved to document genuine change, although the specific data should be consulted. Furthermore, variability and reproducibility are improved if a single experienced operator/observer acquires and measures serial scans.
Background Exercise‐associated cardiac rhythm disturbances are common, but there is a lack of evidence‐based criteria on which to distinguish clinically relevant rhythm disturbances from those that are not. Objectives To describe and characterise rhythm disturbances during clinical exercise testing; to explore potential risk factors for these rhythm disturbances and to determine whether they influenced future racing. Study design Retrospective cohort using a convenience sample. Methods Medical records were reviewed from two clinical services to identify horses with poor performance and/or respiratory noise with both exercise endoscopy and electrocardiography results. Respiratory and ECG findings recorded by the attending clinicians were described, and for polymorphic ventricular rhythms (n = 12), a consensus team agreed the final rhythm characterisation. Several statistical models analysing risk factors were built and racing records were reviewed to compare horses with and without rhythm disturbance. Results Of 245 racehorses, 87 (35.5%) had no ectopic/re‐entrant rhythms, 110 (44.9%) had isolated premature depolarisations during sinus rhythm and 48 (19.6%) horses had complex tachydysrrythmias. Rhythm disturbances were detected during warm‐up in 20 horses (8.2%); during gallop in 61 horses (24.9%) and during recovery in 124 horses (50.6%). Most complex rhythm events occurred during recovery, but there was one horse with a single couplet during gallop and another with a triplet during gallop. Fifteen horses (one with frequent isolated premature depolarisations and 14 complex rhythms) were considered by clinicians to be potentially contributing to poor performance. Treadmill exercise tests, the presence of exercise‐associated upper respiratory tract obstructions and National Hunt racehorses were associated with rhythm disturbances. The proportion of horses racing again after diagnosis (82%) was similar in all groups and univariable analysis revealed no significant associations between subsequent racing and the presence of any ectopic/re‐entrant rhythm, or the various sub‐groups based on phase of exercise in which this was detected. Main limitations Reliance on retrospective data collection from medical records with no control group. Exercise ECGs were collected using only 1 or 2 leads. Variables examined as risk factors could be considered to be inter‐related and our sub‐groups were small. Conclusions This study confirms a high prevalence of cardiac rhythm disturbances, including complex ectopic/re‐entrant rhythms, in poorly performing racehorses. Detection of rhythm disturbances may vary with exercise test conditions and exercise‐associated upper respiratory tract obstructions increase the risk of rhythm disturbances.
Dogs with congestive heart failure had a statistically significant increase in neutrophils, band neutrophils and monocytes in comparison with those without cardiac disease but the cell counts remained within normal reference intervals.
Background Infective endocarditis (IE) in dogs is associated with severe disease and a high case fatality rate but often presents with nonspecific clinical signs. Hypothesis/Objectives Serum concentration of cardiac troponin‐I (cTnI) is elevated in dogs with IE and can differentiate dogs with IE from dogs with other diseases with similar clinical features. Concentration of serum cTnI is negatively correlated with survival time in dogs with IE. Animals Seventy‐two client‐owned dogs; 29 with IE, 27 with stage‐B myxomatous mitral valve disease (MMVD), and 16 with immune‐mediated disease (IMD). Methods Retrospective clinical cohort study. Concentration of serum cTnI was measured in all dogs at time of diagnosis. Clinical findings and echocardiographic interpretation were also recorded. Statistical analyses included Kruskal‐Wallis test, pairwise Mann‐Whitney U tests, receiver operator characteristic, and Cox proportional hazards. Results Serum concentration of cTnI was significantly higher in the IE group (0.69 ng/mL [0.03‐80.8]) than in the MMVD (0.05 ng/mL [0.02‐0.11], P < .001) and IMD groups (0.05 ng/mL [0.03‐0.57], P < .001). Increased cTnI was a moderately accurate predictor of IE (area under the curve 0.857 (95% confidence interval [CI] 0.745‐0.968, P < .001). A cTnI cutoff of 0.625 ng/mL had 100% specificity (95% CI 90%‐100%) and 52% sensitivity (95% CI 33%‐70%) in this study sample. There was no association between cTnI concentration and survival time in dogs with IE (hazard ratio 1.013, 95% CI 0.993‐1.034, P = .2). Conclusions and Clinical Importance Cardiac troponin‐I concentrations are higher in dogs with IE compared to dogs with preclinical MMVD or IMD. In dogs with a compatible clinical presentation, serum cTnI concentrations >0.625 ng/mL are supportive of IE.
Background: Studies describing the clinical progression of animals with reverse patent ductus arteriosus (PDA) are lacking. Objectives: To describe the signalment, presenting signs, echocardiographic features, and survival in a group of dogs and cats with bidirectional and continuous right-to-left PDA. Animals: Forty-six client-owned animals included, comprising 43 dogs and 3 cats with bidirectional or continuous right-to-left PDA. Methods: Retrospective multicenter study. Medical records and echocardiographic findings reviewed from animals diagnosed with bidirectional or continuous right-toleft PDA. Impact of ductal morphology, spectral Doppler flow profile, PCV, sildenafil treatment at presentation, sildenafil dose, severity of pulmonary hypertension, general anesthesia with or without surgery and the presence of right-sided congestive heart failure (R-CHF) on crude mortality rate were evaluated via Mantel-Cox log rank comparison of Kaplan-Meier survival curves. Univariable and multivariable Cox proportional hazards analysis was performed, and hazard ratio (HR) (95% confidence intervals [CI]) was presented. Results: Hindlimb collapse was the most common presenting sign in dogs (n = 16). Clinical signs in cats were variable. Median survival time was 626 days in dogs (range 1-3628 days). Dogs with R-CHF had a shorter median survival time (58 days vs 1839 days, P = .03). Dogs treated with sildenafil at initial presentation survived longer (1839 days vs 302 days, P = .03), which was the only independent predictor of survival (HR 0.35, CI 0.15-0.86, P = 0.021).
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