Use of combined cutting balloon and high-pressure balloon technique for the treatment of double-chambered right ventricle or primary infundibular stenosis: a case series.

Five dogs and two cats with a diagnosis of double-chambered right ventricle or primary infundibular stenosis were referred to undergo a combined cutting balloon and high-pressure balloon technique. At admission five cases were asymptomatic, one had a history of syncope and one had signs of right-sided congestive heart failure. Each patient underwent a complete transthoracic echocardiogram, thoracic radiographs, an angiogram and the combined interventional procedure. Median diameter of the right mid-ventricular stenosis was 4 mm (range 2-8.7 mm) in dogs, and it measured 1.9 and 2 mm in cats. Under general anesthesia initial dilation with an 8-mm × 2-cm cutting balloon was performed from a left external jugular vein approach followed by dilation with a high-pressure balloon (1.5:1 balloon diameter-right outflow tract diameter ratio). In one dog and the two cats the procedure was not completed due to technical issues. In the other four dogs the median intracavitary proximal chamber pressure decreased from 100 mmHg (range 70-150 mmHg) before the procedure to 57 mmHg (range 45-70 mmHg) post-dilation. Long-term follow-up (from six months to two years) showed complete or partial reverse remodeling of the proximal chamber with a median residual pressure gradient below 80 mmHg (range 46-75 mmHg) for all four dogs. This case series shows that this procedure should be considered in dogs with right ventricular outflow tract obstruction. In cats, the procedure might be feasible, if additional guidewire inventory were available.

R-peak time in clinically healthy dogs with different thoracic conformations.

R-peak time (RPT) is an electrocardiographic parameter that represents the time taken for electrical activation to spread from the endocardium to the epicardium. In human medicine, right ventricular RPT is measured from lead V1 to lead V2, and left ventricular RPT from lead V5 to lead V6. The aim of the present study was to define RPT duration in a group of clinically healthy dogs with different thoracic conformations. Sixty clinically healthy dogs underwent a 12-lead electrocardiogram recorded using a previously described precordial system. The dogs were allocated into three morphologic groups. In the brachymorphic group, the median and 25th-75th percentiles for RPT in V1 were 10.5 ms (10-12 ms); V2, 18 ms (16.5-20 ms); V3, 19 ms (18-22 ms); V4, 20 ms (17-23.5 ms); V5, 21 ms (18.5-24 ms); and V6: 22 ms (18.5-25.5 ms). In the mesomorphic group, RPT in V1 was 16 ms (14-18 ms); V2, 22 ms (20-24 ms); V3, 23 ms (21-25 ms); V4, 23 ms (22-25 ms); V5, 25 ms (23-27 ms); and V6, 28 ms (25-30 ms). In the dolichomorphic group, RPT in V1 was 15 ms (13-17 ms); V2, 29 ms (26-32.5 ms); V3, 30 ms (27-33.5 ms); V4, 29.5 ms (26-35 ms); V5, 30 ms (28-34 ms); and V6, 31.5 ms (28-35 ms). RPT in V1 was significantly shorter than RPT in V2 to V6 in all morphotypes (P < 0.05). In all precordial leads, RPT was significantly different between morphotypes (P < 0.05). These results are in agreement with previous findings in humans and with the observation that V1 reads the right ventricle and V2 to V6 read the left ventricle. These preliminary data provide RPT ranges in clinically healthy dogs of different morphotypes.

The predictive value of clinical, radiographic, echocardiographic variables and cardiac biomarkers for assessing risk of the onset of heart failure or cardiac death in dogs with preclinical myxomatous mitral valve disease enrolled in the DELAY study.

OBJECTIVES: To identify the predictive value on time to onset of heart failure (HF) or cardiac death of clinical, radiographic, and echocardiographic variables, as well as cardiac biomarkers N-terminal pro brain natriuretic peptide (NT-proBNP) and cardiac troponin I in dogs with preclinical myxomatous mitral valve disease (MMVD). ANIMALS: One hundred sixty-eight dogs with preclinical MMVD and left atrium to aortic root ratio ≥1.6 (LA:Ao) and normalized left ventricular end-diastolic diameter ≥1.7 were included. METHODS: Prospective, randomized, multicenter, single-blinded, placebo-controlled study. Clinical, radiographic, echocardiographic variables and plasma cardiac biomarkers concentrations were compared at different time points. Using receiving operating curves analysis, best cutoff for selected variables was identified and the risk to develop the study endpoint at six-month intervals was calculated. RESULTS: Left atrial to aortic root ratio >2.1 (hazard ratio [HR] 3.2, 95% confidence interval [95% CI] 1.9-5.6), normalized left ventricular end-diastolic diameter > 1.9 (HR: 6.3; 95% CI: 3.3-11.8), early transmitral peak velocity (E peak) > 1 m/sec (HR: 3.9; 95% CI: 2.3-6.7), and NT-proBNP > 1500 ρmol/L (HR: 5.7; 95% CI: 3.3-9.5) were associated with increased risk of HF or cardiac death. The best fit model to predict the risk to reach the endpoint was represented by the plasma NT-proBNP concentrations adjusted for LA:Ao and E peak. CONCLUSIONS: Logistic and survival models including echocardiographic variables and NT-proBNP can be used to identify dogs with preclinical MMVD at higher risk to develop HF or cardiac death.

Electrophysiologic characteristics and topographic distribution of focal atrial tachycardias in dogs.

BACKGROUND: Focal atrial tachycardia (FAT) is a common supraventricular tachycardia in dogs. OBJECTIVE: To evaluate electrophysiologic characteristics and topographic distribution of FAT. ANIMALS: Sixteen dogs with symptomatic FAT. METHODS: Retrospective case series. Electrophysiological studies were performed to test the inducibility of documented and no documented arrhythmias. Once induced for each dog, FAT was analyzed for electrogenic mechanism, endocardial electrogram, and location. RESULTS: Nineteen FATs could be studied in 16 dogs, 12 were automatic, 4 nonautomatic, and 3 incessant. Two dogs had >1 focus. Mean atrial cycle length (CL) was 238.2 +/- 69.2 (SD) milliseconds, mean ventricular CL of 292.7 +/- 72.5 (SD) milliseconds, with atrioventricular block in 6 cases. Mean presystolic atrial activity recorded at the ectopic focus was -39.9 +/- 17.7 (SD) milliseconds. Atrial potentials were fragmented in 11 dogs and were low amplitude in 6 dogs. Sixty-three percent of ectopic foci were distributed within the right atrium (5 crista terminalis, 3 triangle of Koch, 2 tricuspid valve annulus, 1 interatrial septum, and 1 right auricle) and 37% in the pulmonary veins (PVs) (4 right superior PV, 2 left superior PV, and 1 right inferior PV). Persistent atrial fibrillation (AF) and paroxysmal AF were triggered by FATs in 7 dogs (2 with multiple ectopic foci and 4 with at least one PV focus). CONCLUSION AND CLINICAL RELEVANCE: According to our findings, dogs have a predominance of right-sided FAT. The majority of FATs are automatic and can trigger AF, particularly in the case of PV location.

Heart rhythm characterisation during unexplained transient loss of consciousness in dogs.

The identification of the heart rhythm during an episode of transient loss of consciousness (TLOC) is considered the reference standard method to elucidate the underlying aetiology. This study aimed to characterise heart rhythm in dogs during TLOC using Holter and external loop recorder monitoring. We retrospectively reviewed 24-h Holter monitoring and external loop recorder tracings from 8084 dogs. Heart rhythms from dogs that experienced TLOC during the recording was analysed to identify rhythm disturbances that occurred during episodes of TLOC. Electrocardiograms (ECGs) were subsequently categorised into Type 1 (ventricular arrest), Type 2 (sinus bradycardia), Type 3 (no/slight rhythm variations), and Type 4 (tachycardia). Transient LOC was documented in 92 dogs over 230 episodes of TLOC. Percentage of cases with ECGs compatible with each classification were as follows: 72.1%, Type 1; 6.1%, Type 2; 20.9%, Type 3; and 0.9%, Type 4. Cardiac rhythm during the TLOC could have been a consequence of a neurocardiogenic mechanism in 46.7% cases, while intrinsic rhythm disturbances of the sinus node or of the atrioventricular node were diagnosed in 31.5% cases. In two cases, tachycardia was the possible cause of the TLOC. ECG patterns in dogs presenting with multiple TLOC episodes were completely reproducible during each episode. TLOC in dogs was primarily caused by ventricular arrest. Most dogs with TLOC had electrocardiographic finding suggestive of a reflex or neurally-mediated syncope, but one third had an ECG more suggestive of a conduction disorder. Distinguishing these two entities could help inform diagnostic, therapeutic, and prognostic plans.

DELay of Appearance of sYmptoms of Canine Degenerative Mitral Valve Disease Treated with Spironolactone and Benazepril: the DELAY Study.

INTRODUCTION: Efficacy of renin-angiotensin-aldosterone system (RAAS) blockade using angiotensin-converting enzyme inhibitors (ACEi) in dogs with preclinical myxomatous mitral valve disease (MMVD) is controversial. HYPOTHESIS: Administration of spironolactone (2-4 mg q 24 h) and benazepril (0.25-0.5 mg q 24 h) in dogs with preclinical MMVD, not receiving any other cardiac medications, delays the onset of heart failure (HF) and cardiac-related death. Moreover, it reduces the progression of the disease as indicated by echocardiographic parameters and level of cardiac biomarkers N-terminal pro brain natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI). ANIMALS: 184 dogs with pre-clinical MMVD and left atrium-to-aortic root ratio (LA:Ao) ≥1.6 and normalized left ventricular end-diastolic diameter (LVEDDn) ≥1.7. METHODS: This is a prospective, randomized, multicenter, single-blinded, placebo-controlled study. Primary outcome variable was time-to-onset of first occurrence of HF or cardiac death. Secondary end points included effect of treatment on progression of the disease based on echocardiographic and radiographic parameters, as well as variations of NT-proBNP and cTnI concentrations. RESULTS: The median time to primary end point was 902 days (95% confidence interval (CI) 682-not available) for the treatment group and 1139 days (95% CI 732-NA) for the control group (p = 0.45). Vertebral heart score (p = 0.05), LA:Ao (p < 0.001), LVEDDn (p < 0.001), trans-mitral E peak velocity (p = 0.011), and NT-proBNP (p = 0.037) were lower at the end of study in the treatment group. CONCLUSIONS: This study failed in demonstrating that combined administration of spironolactone and benazepril delays onset of HF in dogs with preclinical MMVD. However, such treatment induces beneficial effects on cardiac remodeling and these results could be of clinical relevance.

Indications for permanent pacing in dogs and cats.

Pacemaker implantation is considered as a standard procedure for treatment of symptomatic bradycardia in both dogs and cats. Advanced second-degree and third-degree atrioventricular blocks, sick sinus syndrome, persistent atrial standstill, and vasovagal syncope are the most common rhythm disturbances that require pacing to either alleviate clinical signs or prolong survival. Most pacemakers are implanted transvenously, using endocardial leads, but rarely epicardial leads may be necessary. To decide whether a patient is a candidate for pacing, as well as which pacing modality should be used, the clinician must have a clear understanding of the etiology, the pathophysiology, and the natural history of the most common bradyarrhythmias, as well as what result can be achieved by pacing patients with different rhythm disturbances. The goal of this review was, therefore, to describe the indications for pacing by evaluating the available evidence in both human and veterinary medicine. We described the etiology of bradyarrhythmias, clinical signs and electrocardiographic abnormalities, and the choice of pacing modality, taking into account how different choices may have different physiological consequences to selected patients. It is expected that this review will assist veterinarians in recognizing arrhythmias that may require permanent pacing and the risk-benefit of each pacing modality and its impact on outcome.

Aortic dissection in four cats: clinicopathological correlations.

Aortic dissection (AD) is characterized by bleeding within the aortic wall or a tear in the intimal layer of the aortic wall, resulting in the passage of blood from the aortic lumen into the tunica media. In cases of AD, a floating, intimal flap in the aortic lumen divides the lumen into a true portion, with flow present, and a false portion, with no flow. We describe a series of 4 cats with AD of the ascending aorta and moderate aortic insufficiency. Three cats had an acute onset of clinical signs with pericardial effusion and cardiac tamponade, whereas one cat showed a chronic onset without pericardial effusion. Detailed gross and histopathological characterization is available for two cats, which revealed the typical features of AD. One cat also showed connective tissue abnormalities, microscopically resembling Marfan-like syndrome. Concomitant detection of hypertrophic cardiomyopathy in 2 cats represents a novel finding in the veterinary literature. Feline AD is generally associated with systemic hypertension. In all the cats of this case series, blood pressure was normal at presentation, although systemic hypertension before the acute dissection cannot be ruled out. In humans, hypotension is more common with AD of the ascending aorta, so the anatomical location could also play a role in cats. Hypertrophic cardiomyopathy in cats could have been a potential trigger of AD through shear stress. Transthoracic echocardiography, as herein demonstrated, can be considered as a rapid, non-invasive and useful method for the diagnosis of dissection at the level of the ascending aorta.

Utility of 12-lead electrocardiogram for differentiating paroxysmal supraventricular tachycardias in dogs.

BACKGROUND: The 12-lead surface ECG is validated for differentiating supraventricular tachycardias (SVT) in humans. Despite the description of SVT in veterinary medicine, no studies have analyzed the electrocardiographic features of this type of arrhythmias in dogs. OBJECTIVE: To describe the specific electrocardiographic criteria used to differentiate the most common SVT in dogs. ANIMALS: Twenty-three dogs examined at Clinica Veterinaria Malpensa for SVT with the mechanism documented by electrophysiologic studies (EPS). METHODS: Twelve-lead electrocardiographic variables obtained from 14 dogs with orthodromic atrioventricular reciprocating tachycardia (OAVRT) and 9 dogs with focal atrial tachycardia (FAT) were compared. RESULTS: Dogs with FAT had faster heart rates (278 +/- 62 versus 229 +/- 42 bpm; P= .049) and less QRS alternans (33 versus 86%; P= .022). P waves appeared during tachycardia in 22 dogs, with a superior axis in 100% of OAVRT and 22% of FAT (P < .001). OAVRT was characterized by a shorter RP interval (85.0 +/- 16.8 versus 157.1 +/- 37.3 ms; P < .001) and smaller RP/PR ratio (0.60 +/- 0.18 versus 1.45 +/- 0.52; P < .001). Repolarization anomalies were present in 64% of OAVRT and no FAT (P < .001). Multivariate analysis identified QRS alternans and a positive P wave in aVR during tachycardia as independent predictors of arrhythmia type. CONCLUSION AND CLINICAL IMPORTANCE: Electrocardiographic criteria used in people for differentiating SVT can also be applied in dogs.

Survival characteristics and prognostic variables of dogs with mitral regurgitation attributable to myxomatous valve disease.

BACKGROUND: There are few studies evaluating the natural history and prognostic variables in chronic mitral valve disease (CMVI) in a heterogeneous population of dogs. OBJECTIVES: To estimate survival and prognostic value of clinical and echocardiographic variables in dogs with CMVI of varying severity. Five hundred and fifty-eight dogs belonging to 36 breeds were studied. METHODS: Dogs were included after clinical examination and echocardiography. Long-term outcome was assessed by telephone interview with the owner. RESULTS: The mean follow-up time was 22.7 +/- 13.6 months, and the median survival time was 19.5 +/- 13.2 months. In univariate analysis, age>8 years, syncope, HR>140 bpm, dyspnea, arrhythmias, class of heart failure (International Small Animal Cardiac Health Council), furosemide therapy, end-systolic volume-index (ESV-I)>30 mL/m(2), left atrial to aortic root ratio (LA/Ao)>1.7, E wave transmitral peak velocity (Emax)>1.2 m/s, and bilateral mitral valve leaflet engagement were associated with survival time when all causes of death were included. For the cardiac-related deaths, all the previous variables except dyspnea and EDV-I>100 mL/m(2) were significantly associated with survival time. Significant variables in multivariate analysis (all causes of death) were syncope, LA/Ao>1.7 m/s, and Emax>1.2 m/s. For cardiac-related death, the only significant variable was LA/Ao>1.7. CONCLUSIONS AND CLINICAL IMPORTANCE: Mild CMVI is a relatively benign condition in dogs. However, some clinical variables can identify dogs at a higher risk of death; these variables might be useful to identify individuals that need more frequent monitoring or therapeutic intervention.

Effect of pimobendan or benazepril hydrochloride on survival times in dogs with congestive heart failure caused by naturally occurring myxomatous mitral valve disease: the QUEST study.

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 = 0.688, 95% confidence limits [CL]=0.516-0.916, P= .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.

Transient myocardial thickening in a Bartonella henselae-positive cat.

A 3-year-old castrated male domestic shorthair presented to the Cornell University Hospital for Animals for acute onset respiratory distress. Thoracic radiographs, echocardiogram, and electrocardiogram (ECG) revealed left-sided congestive heart failure, myocardial thickening with left atrial dilation, and sinus rhythm conducted with a left bundle branch block, respectively. Cardiac troponin I was elevated and continued to increase over 36 h (1.9 ng/mL, 3.1 ng/mL, and 3.5 ng/mL, sequentially every 12 h). The cat tested positive for Bartonella henselae and was treated with azithromycin (30 mg/kg by mouth (PO) every 24 h for 30 days), along with furosemide (1 mg/kg PO every 24 h), benazepril (0.4 mg/kg PO every 24 h), pimobendan (0.23 mg/kg PO every 12 h), and clopidogrel (18.75 mg PO every 24 h). Reevaluation at 6 weeks revealed normal respiratory rate on physical examination, normal cardiac structures and function on echocardiogram, resolution of left bundle branch block on ECG, and normal cardiac troponin I levels (0.06 ng/mL). All medications were discontinued at this time, and the cat continued to do well 5 months after reevaluation. Here, we report a case of transient myocardial thickening in a cat that was also positive for B. henselae.

Radiofrequency catheter ablation of accessory pathways in the dog: the Italian experience (2008-2016).

INTRODUCTION: Accessory pathways (APs) in dogs are mostly right-sided, display nondecremental conduction, and mediate atrioventricular reciprocating tachycardias (AVRTs). Radiofrequency catheter ablation (RFCA) is considered the first-line therapy in human patients to abolish electrical conduction along APs. ANIMALS: Seventy-six consecutive client-owned dogs. MATERIAL AND METHODS: Retrospective study to describe the precise anatomical distribution and the electrophysiologic characteristics of APs in a large population of dogs and to evaluate long-term success and complication rates of RFCA. RESULTS: Eighty-three APs were identified in 76 dogs (92.1% with single APs and 7.9% with multiple APs); 96.4% were right-sided, 3.6% left-sided. Conduction along the APs was unidirectional and retrograde in 68.7% of the cases and bidirectional in 31.3%. Accessory pathways presented retrograde decremental properties in 6.5% of the cases. They mediated orthodromic AVRT in 92.1% of the cases and permanent junctional reciprocating tachycardia in 6.5%. In one case, no AVRT could be induced. In 97.4% of dogs, RFCA was attempted with an acute success rate of 100%. In 7.7% of cases, recurrence of the tachycardia occurred within 18 months, followed by a second definitively successful ablation. A major complication requiring pacemaker implantation was identified in 2.6% of dogs. DISCUSSION: Accessory pathway distribution and electrophysiologic properties in these 76 dogs were similar to previous report. Long-term success and complication rates of RFCA in dogs appeared very similar to results of humans. CONCLUSION: Radiofrequency catheter ablation of APs can be performed with a high success rate and low incidence of complications.

Low-energy ablation of anteroseptal accessory pathways in two dogs.

In humans, accessory pathways (APs) in an anteroseptal and midseptal position are often challenging to ablate because of their close proximity with the conduction pathways of the atrioventricular junction. The use of low-energy ablation techniques can be useful to reduce the risk of permanently damaging the atrioventricular node and the His bundle. This report describes the use of low-energy radiofrequency catheter ablation to successfully and permanently ablate anteroseptal APs in two dogs with orthodromic atrioventricular reciprocating tachycardia. In the first dog, a transient first degree atrioventricular block persisted for 30 s after radiofrequency energy delivery. In the second dog, transient paroxysmal atrioventricular conduction block was observed during the procedure but resolved within 3 days. First degree atrioventricular block was again identified 2 months later. In conclusion, anteroseptal APs can be effectively treated by low-energy radiofrequency catheter ablation with minimal and transient damage to the atrioventricular junction.

Longitudinal Analysis of Quality of Life, Clinical, Radiographic, Echocardiographic, and Laboratory Variables in Dogs with Preclinical Myxomatous Mitral Valve Disease Receiving Pimobendan or Placebo: The EPIC Study.

BACKGROUND: Changes in clinical variables associated with the administration of pimobendan to dogs with preclinical myxomatous mitral valve disease (MMVD) and cardiomegaly have not been described. OBJECTIVES: To investigate the effect of pimobendan on clinical variables and the relationship between a change in heart size and the time to congestive heart failure (CHF) or cardiac-related death (CRD) in dogs with MMVD and cardiomegaly. To determine whether pimobendan-treated dogs differ from dogs receiving placebo at onset of CHF. ANIMALS: Three hundred and fifty-four dogs with MMVD and cardiomegaly. MATERIALS AND METHODS: Prospective, blinded study with dogs randomized (ratio 1:1) to pimobendan (0.4-0.6 mg/kg/d) or placebo. Clinical, laboratory, and heart-size variables in both groups were measured and compared at different time points (day 35 and onset of CHF) and over the study duration. Relationships between short-term changes in echocardiographic variables and time to CHF or CRD were explored. RESULTS: At day 35, heart size had reduced in the pimobendan group: median change in (Δ) LVIDDN -0.06 (IQR: -0.15 to +0.02), P < 0.0001, and LA:Ao -0.08 (IQR: -0.23 to +0.03), P < 0.0001. Reduction in heart size was associated with increased time to CHF or CRD. Hazard ratio for a 0.1 increase in ΔLVIDDN was 1.26, P = 0.0003. Hazard ratio for a 0.1 increase in ΔLA:Ao was 1.14, P = 0.0002. At onset of CHF, groups were similar. CONCLUSIONS AND CLINICAL IMPORTANCE: Pimobendan treatment reduces heart size. Reduced heart size is associated with improved outcome. At the onset of CHF, dogs treated with pimobendan were indistinguishable from those receiving placebo.

Bartonella-associated inflammatory cardiomyopathy in a dog.

A 6-year-old, male, mongrel dog was presented for acute onset of dyspnea and cough. At admission, the dog was cachectic and severely depressed. The electrocardiogram showed a sinus rhythm conducted with left bundle truncular branch block and interrupted by frequent multiform ventricular ectopic beats organized in allorhythmias. Thoracic radiographs revealed a marked cardiomegaly with perihilar edema, whereas transthoracic echocardiography revealed a dilated cardiomyopathy with segmental dyskinesis. Furosemide, enalapril, pimobendan, and mexiletine were prescribed, and a Holter was scheduled after resolution of congestive heart failure. Three days later, the dog died suddenly during sleep. Histopathology revealed diffuse myocyte hypertrophy with multifocal hemorrhages, alternating to areas of severe replacement fibrosis and lymphoplasmocytic infiltrates. Immunohystochemistry stains were strongly positive for T-lymphocyte infiltration (CD3) and weakly positive for B-lymphocytes (CD79). Polymerase chain reaction was positive for Bartonella spp. Based on these results, a post-mortem diagnosis of bacterial inflammatory cardiomyopathy was made.

Long-term Intrinsic Rhythm Evaluation in Dogs with Atrioventricular Block.

BACKGROUND: Atrioventricular block (AVB) is a conduction abnormality along the atrioventricular node that, depending on etiology, may lead to different outcomes. OBJECTIVES: To evaluate variations of intrinsic rhythm (IR) in dogs that underwent pacemaker implantation (PMI). ANIMALS: Medical records of 92 dogs affected by 3rd degree atrioventricular block (3AVB), advanced 2nd degree AVB (2AVB), paroxysmal 3AVB, 2:1 2AVB, or 3AVB with atrial fibrillation (AF) were retrospectively reviewed. METHOD: The patient IR was documented with telemetry on the day of 1--(95% CI, 1-2), 33--(95% CI, 28-35), 105--(95%CI, 98-156), and 275 days (95%CI, 221-380) after PMI. According to AVB grade at different examinations, AVB was defined as progressed, regressed, or unchanged. RESULTS: In 48 dogs, 3AVB remained unchanged, whereas in 7 it regressed. Eight cases of 2AVB progressed, 3 regressed and 2 remained unchanged. Eight cases of paroxysmal 3AVB progressed and 3 remained unchanged. Four dogs affected by 2:1 2AVB progressed, 2 regressed, and 1 remained unchanged. All cases with 3AVB with AF remained unchanged. Regression occurred within 30 days after PMI, whereas progression was documented at any time. Variations in IR were associated with type of AVB (P < .03) and time of follow-up (P < .0001). CONCLUSIONS AND CLINICAL IMPORTANCE: The degree of AVB assessed at the time of PMI should not be considered definitive because more than one-third of the cases in this study either progressed or regressed. Additional studies would be necessary to elucidate possible causes for transient AVB in dogs.

Paroxysmal atrial fibrillation in seven dogs with presumed neurally-mediated syncope.

OBJECTIVES: To document the electrocardiographic findings of vagally-induced paroxysmal atrial fibrillation following a presumed reflex syncopal episode in the dog. ANIMALS: Seven dogs with a syncopal episode followed by a paroxysm of atrial fibrillation recorded on a 24-hour Holter. METHODS: Twenty-four hour Holter monitors were retrospectively reviewed, analysing the cardiac rhythm associated with syncopal events. Each recording was analysed from 10 min before the syncopal episode to until 10 min after a normal sinus rhythm had returned. RESULTS: Nine episodes were recorded in seven dogs, with one patient experiencing three events during one Holter recording. Five of the seven dogs presented with underlying structural heart disease. In two the syncopal episodes occurred following exercise, two associated with coughing and three were during a period of rest. All dogs had documented on the Holter recording a rhythm abnormality during syncope. The most common finding leading up to the syncopal event was development of a progressive sinus bradycardia, followed by sinus arrest interrupted by a ventricular escape rhythm and then ventricular arrest. This was then followed by an atrial fibrillation. The atrial fibrillation was paroxysmal in seven recordings and persistent in two. In two dogs, the atrial fibrillation reorganised into self-limiting runs of atypical atrial flutter. CONCLUSIONS: This combination of electrocardiographic arrhythmias are probably caused by an inappropriate parasympathetic stimulation initiating a reflex or neurally-mediated syncope, with abnormal automaticity of the sinus node and of the subsidiary pacemaker cells and changes in the electrophysiological properties of the atrial muscle, which promoted the paroxysmal atrial fibrillation.

Effect of Pimobendan in Dogs with Preclinical Myxomatous Mitral Valve Disease and Cardiomegaly: The EPIC Study-A Randomized Clinical Trial.

BACKGROUND: Pimobendan is effective in treatment of dogs with congestive heart failure (CHF) secondary to myxomatous mitral valve disease (MMVD). Its effect on dogs before the onset of CHF is unknown. HYPOTHESIS/OBJECTIVES: Administration of pimobendan (0.4-0.6 mg/kg/d in divided doses) to dogs with increased heart size secondary to preclinical MMVD, not receiving other cardiovascular medications, will delay the onset of signs of CHF, cardiac-related death, or euthanasia. ANIMALS: 360 client-owned dogs with MMVD with left atrial-to-aortic ratio ≥1.6, normalized left ventricular internal diameter in diastole ≥1.7, and vertebral heart sum >10.5. METHODS: Prospective, randomized, placebo-controlled, blinded, multicenter clinical trial. Primary outcome variable was time to a composite of the onset of CHF, cardiac-related death, or euthanasia. RESULTS: Median time to primary endpoint was 1228 days (95% CI: 856-NA) in the pimobendan group and 766 days (95% CI: 667-875) in the placebo group (P = .0038). Hazard ratio for the pimobendan group was 0.64 (95% CI: 0.47-0.87) compared with the placebo group. The benefit persisted after adjustment for other variables. Adverse events were not different between treatment groups. Dogs in the pimobendan group lived longer (median survival time was 1059 days (95% CI: 952-NA) in the pimobendan group and 902 days (95% CI: 747-1061) in the placebo group) (P = .012). CONCLUSIONS AND CLINICAL IMPORTANCE: Administration of pimobendan to dogs with MMVD and echocardiographic and radiographic evidence of cardiomegaly results in prolongation of preclinical period and is safe and well tolerated. Prolongation of preclinical period by approximately 15 months represents substantial clinical benefit.

Prevalence and prognostic importance of pulmonary hypertension in dogs with myxomatous mitral valve disease.

BACKGROUND: Pulmonary hypertension (PH) is common in dogs with myxomatous mitral valve disease (MMVD) but its effect on clinical outcome has not been investigated. HYPOTHESIS/OBJECTIVES: The presence of PH worsens the outcome in dogs with MMVD. To compare survival times of dogs with MMVD and PH to those without PH. ANIMALS: Two hundred and twelve client-owned dogs. METHODS: Case review study. Medical records of dogs diagnosed with ACVIM stage B2 and C MMVD between January 2010 and December 2011 were retrospectively reviewed. Long-term outcome was determined by telephone interview or from the medical record. End of the observation period was March 2013. PH was identified if tricuspid regurgitation peak velocity was >3 m/s. RESULTS: Two hundred and twelve were identified. Eighty-three dogs (39%) had PH. PH was more commonly identified in stage C compared to B2 (P < .0001). One hundred and five (49.5%) dogs died during the observation period. Median survival time for the entire study population was 567 days (95% CI 512-743). Stage C (P = .003), the presence of PH (P = .009), left atrial to aortic root ratio (LA/Ao) >1.7 (P = .0002), normalized left-ventricular end-diastolic diameter (LVEDn) >1.73 (P = .048), and tricuspid regurgitation pressure gradient (TRPG) >55 mmHg (P = .009) were associated with worse outcomes in the univariate analyses. The presence of TRPG >55 mmHg (HR 1.8 95% CI 1-2.9; P = .05) and LA/Ao > 1.7 (HR 2 95% CI 1.2-3.4; P = .01) remained significant predictors of worse outcome in the multivariate analysis. CONCLUSIONS AND CLINICAL IMPORTANCE: In dogs with MMVD, moderate to severe PH worsens outcome.