Background: Myxomatous mitral valve disease (MMVD) continues to be an important cause of morbidity and mortality in geriatric dogs despite conventional therapy.Hypothesis: Pimobendan in addition to conventional therapy will extend time to sudden cardiac death, euthanasia for cardiac reasons, or treatment failure when compared with conventional therapy plus benazepril in dogs with congestive heart failure (CHF) attributable to MMVD.Animals: Two hundred and sixty client-owned dogs in CHF caused by MMVD were recruited from 28 centers in Europe, Canada, and Australia.Methods: A prospective single-blinded study with dogs randomized to PO receive pimobendan (0.4-0.6 mg/kg/d) or benazepril hydrochloride (0.25-1.0 mg/kg/d). The primary endpoint was a composite of cardiac death, euthanized for heart failure, or treatment failure.Results: Eight dogs were excluded from analysis. One hundred and twenty-four dogs were randomized to pimobendan and 128 to benazepril. One hundred and ninety dogs reached the primary endpoint; the median time was 188 days (267 days for pimobendan, 140 days for benazepril hazard ratio 5 0.688, 95% confidence limits [CL] 5 0.516-0.916, P 5 .0099). The benefit of pimobendan persisted after adjusting for all baseline variables. A longer time to reach the endpoint was also associated with being a Cavalier King Charles Spaniel, requiring a lower furosemide dose, and having a higher creatinine concentration. Increases in several indicators of cardiac enlargement (left atrial to aortic root ratio, vertebral heart scale, and percentage increase in left ventricular internal diameter in systole) were associated with a shorter time to endpoint, as was a worse tolerance for exercise.Conclusions and Clinical Importance: Pimobendan plus conventional therapy prolongs time to sudden death, euthanasia for cardiac reasons, or treatment failure in dogs with CHF caused by MMVD compared with benazepril plus conventional therapy.

BackgroundThe benefit of pimobendan in delaying the progression of preclinical dilated cardiomyopathy (DCM) in Dobermans is not reported.HypothesisThat chronic oral administration of pimobendan to Dobermans with preclinical DCM will delay the onset of CHF or sudden death and improve survival.AnimalsSeventy-six client-owned Dobermans recruited at 10 centers in the UK and North America.MethodsThe trial was a randomized, blinded, placebo-controlled, parallel group multicenter study. Dogs were allocated in a 1:1 ratio to receive pimobendan (Vetmedin capsules) or visually identical placebo.The composite primary endpoint was prospectively defined as either onset of CHF or sudden death. Time to death from all causes was a secondary endpoint.ResultsThe proportion of dogs reaching the primary endpoint was not significantly different between groups (P = .1). The median time to the primary endpoint (onset of CHF or sudden death) was significantly longer in the pimobendan (718 days, IQR 441–1152 days) versus the placebo group (441 days, IQR 151–641 days) (log-rank P = 0.0088). The median survival time was significantly longer in the pimobendan (623 days, IQR 491–1531 days) versus the placebo group (466 days, IQR 236–710 days) (log-rank P = .034).Conclusion and Clinical ImportanceThe administration of pimobendan to Dobermans with preclinical DCM prolongs the time to the onset of clinical signs and extends survival. Treatment of dogs in the preclinical phase of this common cardiovascular disorder with pimobendan can lead to improved outcome.

Myocardial motion was quantified in normal cats (n = 25) and cats with hypertrophic cardiomyopathy (HCM) (n = 23) using the pulsed tissue Doppler imaging (TDI) technique. A physiologic nonuniformity was documented in the myocardial motion of normal cats, which was detected as higher early diastolic velocities, acceleration, and deceleration in the interventricular septum compared with the left ventricular free wall (LVFW). HCM cats exhibited lower early diastolic velocities, acceleration, and deceleration and also prolonged isovolumic relaxation time compared with normal cats. These differences were detected mainly along the longitudinal axis of the heart. A cutoff value of E' in the LVFW along the longitudinal axis >7.2 cm/s discriminated normal from HCM cats with a sensitivity of 92% and a specificity of 87%. The physiologic nonuniformity of myocardial motion during diastole was lost in affected cats. Systolic impairment (decreased late-systolic velocities in most segments along the longitudinal axis and decreased early systolic acceleration in both mitral annular sites) was evident in HCM cats irrespective of the presence of left ventricular outflow tract obstruction and congestive heart failure. Postsystolic thickening was recorded in the LVFW along the longitudinal axis only in affected cats (n = 6) and was another finding indicative of systolic impairment in the HCM of this species. This study identified both diastolic and systolic impairment in cats with HCM compared with normal cats. The study also documents the normal physiologic nonhomogeneity in myocardial motion in cats and the subsequent loss of this feature in the HCM diseased state.

This paper describes the clinical features, and diagnostic findings of a chronic respiratory condition in 29 West Highland white terriers. Typically, the dogs were coughing chronically, had dyspnoea and tachypnoea of varying severity, and had deteriorated progressively over months to years. The mean (sem) survival time in months from the clinical signs being first noted by the owners was 17.9 (2.3). Most cases had a combination of respiratory signs, but coughing was the predominant sign in 18 cases. Inspiratory crackles were audible on chest auscultation in 28 cases, 10 of which were also wheezing. Rhonchi were the predominant sound in the remaining case. The main radiographic changes were mild to severe increased Interstitial markings in all cases, with additional bronchial markings in 14 of the dogs. Right-sided cardiomegaly (cor pulmonale) was recorded in 15. Bronchoscopic findings in 17 of the dogs were either normal or involved a mild airway mucoid reaction in eight. Chronic mucosal changes were observed in eight, but in two this finding was equivocal. Dynamic changes to the lumen of the airway were present in seven cases. No significant haematological or biochemical changes could be detected in 20 cases, but four cases were hypercholestrolaemic. A histopathological assessment of four cases revealed alveolar septal fibrosis to be the predominant change. Prednisolone, with or without bronchodilators, was the most commonly used therapy, and the response was variable. The condition appears to be associated with significant pulmonary interstitial fibrosis of unknown aetiology and has clinical similarities to idiopathic pulmonary fibrosis (cryptogenic fibrosing alveolitis) in human beings.

The case records of 98 dogs with a left-to-right shunting patent ductus arteriosus (PDA) were reviewed. There were 35 breeds represented, with a female to male ratio of 3:1. Forty per cent of the dogs were older than one year at initial presentation and 31 per cent had clinical signs attributable to PDA. A left heart base continuous murmur of grade IV/VI or higher was noted in 90 per cent of the dogs. On electrocardiography, the most common abnormalities were tall R waves (63 per cent) and deep QII waves (62 per cent). The radiographic triad of dilation of the descending aorta with enlargement of the main pulmonary artery segment and left atrium, typical of PDA, was noted in only 26 per cent of cases. Two-dimensional (2D) and M-mode echocardiography detected left atrial enlargement (35 per cent) and an increased left ventricular diameter in diastole (82 per cent) and systole (84 per cent) as the most common abnormalities. Doppler echocardiography demonstrated increased aortic outflow velocities in 66 per cent of cases. The overall short-term successful outcome in this study was 95 per cent. There was no significant difference between surgical ductal ligation using a standard technique or the Jackson-Henderson technique in terms of survival, occurrence of haemorrhage or residual shunting. The number of interventional procedures used in this study was too low for statistical comparison, but there appeared to be a trend towards a higher rate of residual shunting and a lower fatality rate using a coil occlusion technique.

Medical records of 81 dogs with severe pulmonic stenosis from 2 referral centers were examined retrospectively. Forty dogs underwent balloon valvuloplasty (BV), which was performed by 1 operator, whereas 41 did not. The mean age at latest follow-up was 41.5 months. A statistical comparison of the clinical outcome and survival was performed. Dogs revealing clinical signs at presentation showed a 16-fold increase in risk of death compared with asymptomatic dogs (P < .001). Statistical analyses demonstrated that an increase of 1 mm Hg in transstenotic pressure gradient (PG) at presentation was associated with a 3% increase in hazard rate (P < .001). Thirty-seven dogs survived BV with a median reduction in PG of 46%. The median preoperative PG was 120 mm Hg, and median PG 24 hours postoperatively was 55 mm Hg with a median of 55 mm Hg 6 months post-BV. Twenty (49%) of the non-BV (NBV) dogs remained asymptomatic at last follow-up. Fourteen (34%) of the NBV dogs died or were euthanized because of heart disease related to pulmonic stenosis. Twelve of these dogs died suddenly, whereas only 1 of the BV dogs died suddenly. After adjusting for PG, clinical signs at presentation, and age, BV or dilation was associated with a 53% reduction in hazard rate (P = .005). This study indicates that BV, when performed by an experienced operator, appears to be successful both in alleviating clinical signs and in prolonging survival in dogs with severe pulmonic stenosis.

Activated-myofibroblasts (alpha-SMA-positive cells) were increased and inactive-myofibroblasts (vimentin-positive cells) were reduced in mitral valve leaflets of dogs with MMVD, compared with that of clinically normal dogs. Impact on Human Medicine-This is the first description of spatial and temporal alterations in mitral valve cells of any species with MMVD and has clinical importance in the understanding of disease development in dogs and humans.

Postocclusion survival data from dogs with left-to-right shunting patent ductus arteriosus (PDA) was available from 80 dogs, diagnosed from 1990 to 2000. Of these, 37 had undergone a procedure to close the ductus and were re-evaluated at the time of this study; clinical data from the follow-up examination was compared with that from the original examination. Radiographically, the right ventricle remained apparently enlarged, and the aortic bulge associated with dilation of the descending aorta did not disappear after closure. On M-mode echocardiography, left ventricular chamber diameter in diastole and systole and left ventricular posterior wall in systole decreased significantly. Mitral endocardiosis was a common feature. Residual flow was evident in 46 per cent of the animals. Late closure occurred in 8 per cent of the dogs, and trivial recanalisation in 19 per cent. The maximum survival time postclosure was 168 months and, after non-occlusion, 114 months, suggesting that dogs with PDA follow an unpredictable course. However, there was a significant difference in survival times between the corrected and non-corrected group.