Spontaneous pre-excited supraventricular tachycardias in a Labrador Retriever.

A four-year-old Labrador Retriever was presented for intermittent tachycardia. The electrocardiogram showed sinus rhythm conducted with ventricular pre-excitation and short runs of orthodromic atrioventricular reciprocating tachycardia. Four months later, the rhythm degenerated into a symptomatic sustained tachycardia, suspected to be pre-excited atrial fibrillation, a potentially life-threatening rhythm in the presence of an accessory pathway with a short refractory period. Two days after initiating oral diltiazem, the dog deteriorated and represented with sustained orthodromic atrioventricular reciprocating tachycardia, which was terminated by a precordial chest thump. It proceeded to sinus rhythm with ventricular pre-excitation followed by an episode of pre-excited focal atrial tachycardia. A bolus of lidocaine IV successfully restored sinus rhythm and sotalol treatment was started. The dog clinically recovered but died spontaneously 24 h later. This is the first case report that describes spontaneous pre-excited focal atrial tachycardia.

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.

Gene-expression profiling of endomyocardial biopsies from dogs with dilated cardiomyopathy phenotype.

INTRODUCTION: The employment of advanced molecular biology technologies has expanded the diagnostic investigation of cardiomyopathies in dogs; these technologies have predominantly been performed on postmortem samples, although the recent use of endomyocardial biopsy in living dogs has enabled a better premortem diagnostic approach to study the myocardial injury. ANIMALS, MATERIALS, AND METHODS: Endomyocardial biopsies were collected in nine dogs with a dilated cardiomyopathy phenotype (DCM-p) and congestive heart failure and submitted to histologic examination, next-generation sequencing (NGS), and polymerase chain reaction analysis. Data from three healthy dogs (Fastq files) were retrieved from a previously approved study and used as a control group for ribonucleic acid sequencing. RESULTS: Histologic examination revealed endocardial fibrosis in six of nine dogs, whereas lymphocytic interstitial infiltrates were detected in two of nine dogs, and lymphoplasmacytic and macrophage infiltrates were detected in one of nine dogs. On polymerase chain reaction analysis, two dogs tested positive for canine parvovirus two and one dog for canine distemper virus. Gene-expression pathways involved in cellular energy metabolism (especially carbohydrates-insulin) and cardiac structural proteins were different in all DCM-p dogs compared to those in the control group. When dogs with lymphocytic interstitial infiltrates were compared to those in the control group, NGS analysis revealed the predominant role of genes related to inflammation and pathogen infection. CONCLUSIONS: Next-generation sequencing technology performed on in vivo endomyocardial biopsies has identified different molecular and genetic factors that could play a role in the development and/or progression of DCM-p in dogs.

Noninvasive electrocardiographic parameters to assess interventricular dyssynchrony in dogs with bundle branch blocks.

OBJECTIVES: To define electrocardiographic features of complete left bundle branch block (LBBB) and right bundle branch block (RBBB), and the use of R-peak time (RPT) to identify interventricular dyssynchrony in dogs with BBB. ANIMALS, MATERIALS AND METHODS: Twelve-lead ECG tracings of 20 dogs with RBBB, 20 with LBBB, and 60 healthy dogs were retrospectively analyzed and RPT was measured in precordial leads. Interventricular dyssynchrony index (IDI) was than calculated. RESULTS: In RBBB, mean electrical axis (MEA) was -111° [-120/-100°], V1RPT was significantly longer (61 ms [55-72 ms]) than left precordial leads RPT (V2:25 ms [22-30 ms]; V3:25 ms [22-29 ms]; V4:24 ms [21-29 ms]; V5:25 ms [22-29 ms]; V6:25 ms [22-29 ms]) and when compared to normal dogs (P < 0.001). In LBBB, MEA was 76° [70/81°], RPT in left precordial leads was significantly longer (V2:49 ms [34-58 ms]; V3:49 ms [43-57 ms]; V4:52 ms [45-62 ms]; V5:53 ms [45-63 ms]; V6:55 ms [45-63 ms]) than V1RPT (17 ms [15-20 ms]) and when compared to normal dogs (P < 0.001). V1RPT > 28 ms and V5RPT > 36 ms were found to predict the presence of RBBB and LBBB with a sensitivity of 100% and 96.7%, and a specificity of 96.7% and 99.5%, respectively. The IDI was 23% [16-29%] in normal dogs and significantly greater in dogs with RBBB (33% [30-38%]; P < 0.001) and LBBB (32% [23-41%]; P = 0.006). CONCLUSIONS: This study defines ECG features and RPT in dogs with BBB. Electrical interventricular dyssynchrony can be defined using IDI in dogs with BBB.

Heart rhythm characterization during sudden cardiac death in dogs.

INTRODUCTION/OBJECTIVES: Inherited or acquired arrhythmic disorders and cardiac disease have been associated with sudden cardiac death (SCD) in dogs. The electrical mechanism related to death in most of these cases is unknown. This retrospective study aimed to describe arrhythmic events in dogs that experienced SCD during Holter monitoring. ANIMALS, MATERIALS AND METHODS: Nineteen client-owned dogs that experienced SCD during Holter examination were included. Clinical records from a Holter service database were reviewed, and both the rhythm preceding death and the dominant rhythm causing SCD were analysed. Clinical data, Holter diaries and echocardiographic diagnosis were also evaluated. RESULTS: Structural heart disease was identified in 12/19 dogs (dilated cardiomyopathy in five dogs, arrhythmogenic right ventricular cardiomyopathy in four dogs, myxomatous mitral valve disease in two dogs, and suspected myocarditis in one dog), five of which had concurrent congestive heart failure. Sudden cardiac death was related to ventricular premature complexes or monomorphic ventricular tachycardia degenerating into ventricular fibrillation in 42% of dogs, polymorphic ventricular tachycardia, or torsade de pointes-like inducing ventricular fibrillation in 21%, and asystole or presumptive agonal pulseless electrical activity triggered by malignant bradyarrhythmias in 37%. CONCLUSIONS: The most common rhythm associated with SCD in our population of dogs was ventricular tachycardia leading to ventricular fibrillation, although bradyarrhythmia-related SCD, possibly related to inappropriate vagal reflexes, was also a notable cause.

Radiofrequency catheter ablation of cranial vena cava flutter in four dogs.

Four dogs were referred to our institution for incessant supraventricular tachycardias causing weakness; congestive heart failure was present in one dog. At admission, all dogs had a surface electrocardiogram showing a narrow QRS complex tachycardia with a ventricular rate ranging from 80 to 300 bpm, variable atrioventricular conduction ratio from 1:1 to 3:1, and positive atrial depolarizations in inferior leads (II, II, III, and aVF), with isoelectric lines between them. Three of four dogs had a dilated cardiomyopathy phenotype; one dog had a heart base tumor involving the cranial vena cava wall. According to the electrocardiographic findings, a presumptive diagnosis of reverse typical or atypical atrial flutter was considered, and endocardial mapping was planned for each dog. During the electrophysiologic study, continuous atrial activation compatible with atypical atrial flutter was observed in all dogs, with concealed entrainment obtained at the level of the isthmus located at the distal portion of the cranial vena cava, close to the entrance into the right atrium. A linear radiofrequency catheter ablation was performed from the right atrial wall to the distal part of the cranial vena cava with a permanent interruption of the isthmic conduction in all dogs at a 6-month follow-up.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.