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.

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.

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.

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.

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.

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.