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Background: Advanced heart failure (AHF) secondary to myxomatous mitral valve disease (MMVD) in dogs has unclear predictive variables and survival time., Methods: This retrospective study included 38 dogs with AHF and 38 with stable congestive heart failure (CHF), both due to MMVD. Predictive variables for AHF were analysed, and survival times were calculated using logistic regression and the Kaplan-Meier method., Results: Left atrium to aortic root ratio, normalised left ventricular dimension at the end-diastole and end-systole, isovolumic relaxation time (IVRT) and early transmitral inflow velocity to IVRT ratio were associated with AHF progression. The median survival times were significantly longer in the stable group than in the AHF group. After AHF diagnosis, the median survival times for all-cause and cardiogenic mortality were 194 and 354 days, respectively., Limitations: This was a single-centre retrospective observational study. The study population was small, with breed bias (overrepresentation of Maltese dogs). Additionally, the treatment plans depended on clinical experience., Conclusions: AHF in dogs with CHF secondary to MMVD is linked to left heart chamber enlargement and increased left ventricular dimensions, significantly reducing survival time to around six months post-diagnosis. Early recognition and appropriate management may improve outcomes, highlighting the importance of advanced treatment strategies., (© 2024 British Veterinary Association.)

Serial measurements of cardiac troponin I (cTnI) levels are considered to be better predictors of cardiac death than single-time-point analyses in human medicine. We hypothesised that cTnI levels could reflect the severity of myxomatous mitral valve disease (MMVD), and that serial changes in the cTnI level had a prognostic value in dogs with congestive heart failure (CHF) secondary to MMVD. Seventy-six dogs were initially enrolled and classified by the American College of Veterinary Internal Medicine (ACVIM) staging system. The single-timepoint cTnI concentration in these dogs significantly increased with the ACVIM stage. Twenty-seven dogs with CHF subsequently underwent serial measurement of cTnI levels, and the results showed that those who demonstrated a decrease in cTnI levels from the first to the third visit exhibited a higher risk of cardiac death than did those without such changes (P=0.012). We suspect that the downward trend in cTnI levels may be affected by medical treatment for CHF. In conclusion, although cTnI levels could reflect the severity of MMVD to a certain extent, the serial changes may be affected by medical treatment. Therefore, caution should be exercised when cTnI is used for assessment of the prognosis of CHF secondary to MMVD in dogs., Competing Interests: Competing interests: None declared., (© British Veterinary Association 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

Time-domain heart rate variability (HRV) parameters and the correlation between echocardiography and Holter examinations in dogs with myxomatous mitral valve disease (MMVD) were determined. Holter examination was also performed at different time frames: an entire 24-hour period, a four-hour period during sleep, and a four-hour period while awake. Ten healthy (control group) and 28 MMVD dogs, 15 with and 13 without heart failure, were evaluated. The SDANN (sd of the mean normal RR intervals for all five-minute segments during 24-hour Holter) and pNN(50) (percentage of differences between adjacent normal RR intervals that are >50 ms computed over 24-hour Holter) variables were significantly lower in the dogs with MMVD heart failure. The differences in HRV between the groups were only detected during the 24-hour evaluation period (P<0.05). There were high correlations (canonical analysis) between Holter and echocardiography examinations when considering pNN(50), SDANN, and LA/AO (left atrial to aortic root ratio) (r=0.92; P<0.05), indicating that both are important in evaluating MMVD dogs. SDANN and pNN(50) are measures of parasympathetic control of the heart, and thus, it is possible to infer that the MMVD dogs exhibit parasympathetic withdrawal during the development of heart failure.

The paper describes the clinical and pathological characteristics of an unusual cystic congenital cardiac anomaly that caused clinical signs of congestive heart failure, respiratory distress and cardiac arrhythmias in two West Highland white terrier puppies. In both dogs a definitive diagnosis was made postmortem.

The endothelin-1 (ET-1) plasma concentration was measured in dogs with spontaneous cardiac or respiratory diseases. Plasma samples were obtained from 76 healthy control dogs and 73 dogs, of which 58 were suffering from heart disease and 15 were suffering from respiratory disease. Dogs were evaluated using echocardiography, thoracic radiography, biochemical evaluation and a radioimmunoassay for ET-1. ET-1 plasma concentrations were significantly higher in dogs with spontaneous cardiac or respiratory diseases (mean [se] 5.3 [0.3] and 5.3 [0.6] pg/ml, respectively) than in healthy dogs (1.9 [0.1] pg/ml) (P<0.0001). ET-1 plasma concentrations increased with the class of heart failure (International Small Animal Cardiac Health Council classification) (P<0.0001) and with the severity of pulmonary disorders. ET-1 plasma concentrations were positively correlated with the extent of systolic pulmonary hypertension measured by Doppler echocardiography (P<0.05; r=0.75) and with the clinical outcome of dogs with respiratory disease. Evaluation of the ET-1 plasma concentration allowed differentiation between heart and respiratory disorders in dogs exhibiting clinical signs at exercise, but not in patients exhibiting clinical signs at rest.

The vasovagal tonus index (VVTI), a time-domain indicator of heart rate variability, was measured in 92 dogs of six breeds (German shepherd dogs, labrador retrievers, cocker spaniels, boxers, bulldogs and cavalier King Charles spaniels). There was a significant difference in VVTI between the six breeds (P = 0.003). Brachycephalic dogs had a higher VVTI than other types of dog (P < 0.005), and when comparing individual breeds brachycephalic breeds tended to have a higher VVTI than non-brachycephalic breeds, although the difference was not always significant. The VVTI was negatively correlated with heart rate (P < 0.01) and dogs suffering from congestive heart failure had a lower VVTI than other dogs, whether compared within or between breeds (P < 0.01).

A six-year-old Staffordshire bull terrier had a four-week history of progressive lethargy, ascites and exercise intolerance. A mass 3 cm in diameter obliterating the right atrial lumen was detected by echocardiographic examination. There were lactescent pericardial and serosanguineous pleural effusions. Histological and immunochemical examinations showed that the mass was a primary rhabdomyoma.

A 17-year-old, 1-kg, colony-housed, male squirrel monkey (Samiri sciureus) developed clinical signs of congestive heart failure. The monkey presented with lethargy, increased heart and respiratory rates, and mild abdominal distention. The clinical history, laboratory analysis, and radiographic findings were consistent with heart failure due to dilative cardiomyopathy. Gross and microscopic examination of the heart confirmed a dilative cardiomyopathy. This is the first report describing congestive heart failure caused by dilative cardiomyopathy in a squirrel monkey. Spontaneous dilative cardiomyopathy may be infrequently observed in the squirrel monkeys because they are not routinely housed in the research environment during their advancing years.

Forty-three horses with mitral regurgitation (MR) and congestive heart failure were examined, using M-mode, 2-dimensional real-time and Doppler echocardiography. There was no breed or sex predisposition when compared to the general hospital population. The mean +/- s.d. age of affected horses was 7.6 +/- 8.1 years. Horses with MR and congestive heart failure had significant increases in mean values for left ventricular chamber size, left atrial size and heart rate and significant decreases in interventricular septal and left ventricular free wall thickness. Significant increases in pulmonary artery diameter were detected compared to aortic diameter. Mean values for fractional shortening were not significantly different from normal. All horses had a Grade 3-6/6 holosystolic or pansystolic murmur with its point of maximal intensity in the mitral to aortic valve area. Atrial fibrillation was found at presentation in 24 horses with MR and congestive heart failure. One horse presented with atrial tachycardia and subsequently developed atrial fibrillation. Seven horses had ventricular premature contractions. Exercise intolerance (n = 34), respiratory signs (n = 31), and fever (n = 21) were the most common presenting signs. Thickening of the left atrioventricular valve leaflets, endocarditis, flail valve leaflets, rupture of a chorda tendineae, and mitral valve prolapse were detected echocardiographically. Doppler echocardiography confirmed the presence of a large systolic regurgitant jet in the left atrium in all horses in which it was used, and in many horses, concurrent tricuspid and pulmonary regurgitation was detected. All horses died or were subjected to euthanasia due to the severity of their MR and/or lack of response to therapy. Post mortem examinations were performed in 35 horses and confirmed the echocardiographic findings. The echocardiographic detection of a flail mitral valve leaflet was significantly associated with the detection of a ruptured chorda tendineae at post mortem examination. There was a significant association between echocardiographic detection of a dilated pulmonary artery and its presence at post mortem examination. M-mode, 2-dimensional real-time, and Doppler echocardiography should be used to accurately characterise the valvular abnormalities and assess the severity of mitral regurgitation. Pulmonary artery dilatation, an echocardiographic indication of severe pulmonary hypertension, should be considered a grave prognostic indicator and may indicate impending pulmonary artery rupture.

Ventricular septal defects (VSDs) were diagnosed in 27 horses; in 26 affected horses systolic murmurs were detected over both sides of the chest. Holodiastolic decrescendo murmurs were also detected in 5 horses. Standardbreds and Arabian horses were over-represented, while Thoroughbred horses were under-represented, when compared to the hospital population (P < 0.0001). Five horses had previously raced successfully, one 2-year-old was training successfully and close to racing, and 4 horses had competed successfully in other types of competition. Eleven horses had a history of exercise intolerance or poor performance, 5 horses were stunted and 3 horses were in congestive heart failure at the time of presentation. The VSD murmur was detected as an incidental finding in 14 horses. Membranous VSD were most commonly detected (in 23/27 affected horses) and were typically found underneath the septal leaflet of the tricuspid valve and the right and/or noncoronary leaflet of the aortic valve. Muscular VSDs were much less common and were located in any portion of the muscular septum. The VSDs ranged in size from 1-4.6 cm (maximal diameter) in affected horses. A left to right shunt through the VSD was detected in 26/27 affected horses with Doppler echocardiography. The peak velocity of shunt flow detected through the VSD was 0-5.8 m/s. The interventricular pressure gradients estimated from the peak shunt velocity obtained with Doppler echocardiography were 0-135 mmHg. Right ventricular pressures estimated with Doppler echocardiography were 15-84 mmHg, similar to invasively obtained measurements of right ventricular pressure in 80% of horses in which right sided cardiac catheterisation was performed (n = 5). Left ventricular and left atrial volume overload was detected in the majority (23/27) of horses. Right atrial and right ventricular volume overload was severe in 3 horses with muscular VSDs, mild in 1 horse with a perimembranous VSD, and mild in 2 horses with membranous VSDs. Concurrent left ventricular dysfunction was detected in 2 horses. Aortic valve prolapse was seen in 7 horses associated with the membranous location of the VSD; 6 of these horses had very mild (1+) or mild (2+) aortic regurgitation. Severe (4+) aortic regurgitation was present in one horse, severe mitral regurgitation in 2 horses, severe tricuspid regurgitation in 3 horses, and severe pulmonary regurgitation was detected in 2 horses. Mitral valve prolapse, tricuspid valve dysplasia, a flail aortic valve leaflet, and a bicuspid pulmonary valve were additional findings detected in one horse each. Post mortem examinations were performed in 8 horses which confirmed the echocardiographic findings. Sixteen out of 27 horses had a history of racing or competing successfully either before or after the diagnosis of the VSD. Two horses were useful pleasure horses, 3 horses presented in congestive heart failure, 1 horse developed signs of congestive heart failure, 2 horses were lost to follow-up and 2 are still alive but are small and stunted. The successful racehorses usually had a membranous VSD that measured < or = 2.5 cm in its largest diameter and a peak velocity of shunt flow through the VSD of > or = 4 m/s. Two-dimensional (2-D) and Doppler echocardiography is useful in assessing the haemodynamic significance of VSDs in horses and can be used to help formulate a prognosis for life and performance.

Chronic constrictive pericarditis was diagnosed in a 6-year-old Thoroughbred mare based on the clinical findings of right congestive heart failure, hyperechoic pericardium without pericardial effusion, and a dip-and-plateau shape of the right ventricular pressure curve with equilibration of the diastolic pressures in all cardiac chambers. Treatment was attempted by partial pericardiectomy using a right lateral thoracotomy approach. Because of severe epicardial involvement recurrence of the constrictive pathology was noted 6 weeks after the surgical procedure. However, in selected cases in which the disease process is limited to the pericardium, partial pericardiectomy may offer a mode of therapy in horses suffering from constrictive pericarditis.

Four dogs with congestive heart failure associated with dirofilariasis and mitral valvular incompetence initially responded to treatment with digoxin or etamiphylline camsylate, and frusemide but became refractory to this therapy and were in cardiac decompensation. Frusemide dosage was increased and the alpha adrenoreceptor blocking drug prazosin hydrochloride was added to the therapeutic regime. Six weeks later all dogs were stabilized and their clinical condition was markedly improved.