Presumed primary cardiac mast cell tumor, pericardial effusion, and arrhythmia in a dog.

A 13-year-old female spayed border collie cross presented for pericardial effusion, arrhythmia, and a suspected cardiac mass. Echocardiogram revealed severe thickening and hypokinesis of the interventricular septum with a heterogenous, cavitated myocardium, concerning for neoplasia. Electrocardiogram revealed predominantly accelerated idioventricular rhythm with frequent periods of nonsustained ventricular tachycardia. Occasional prolonged PR intervals terminating in an aberrantly conducted QRS complex were present. These beats were postulated to represent either first-degree atrioventricular block with aberrant QRS conduction or atrioventricular dissociation. Cytology of the pericardial effusion revealed atypical, suspected neoplastic, mast cells. The patient was euthanized, and postmortem examination confirmed full-thickness infiltration of the interventricular septum by a mast cell tumor, with metastasis to the tracheobronchial lymph node and spleen. Given the anatomic location of the mass, the observed atrioventricular nodal conduction delay may represent neoplastic infiltration of the atrioventricular node. Neoplastic infiltration of the ventricle was suspected to cause the accelerated idioventricular rhythm and ventricular tachycardia. To the authors' knowledge, this is the first reported case of a primary cardiac mast cell tumor causing arrhythmia and pericardial effusion in a dog.

Comparison of the diagnostic value of a small, single channel, electrocardiogram monitoring patch with a standard 3-lead Holter system over 24 hours in dogs.

INTRODUCTION/OBJECTIVES: The aim of this study was to compare a novel small event recorder device, the Carnation Ambulatory Monitor (CAM), with a standard Holter. ANIMALS: Nineteen adult dogs. MATERIAL AND METHODS: Comparative and explorative study. The two devices were simultaneously applied for approximately 24 h. RESULTS: Analysis time (P=0.013) and percentage of artefacts (P<0.001) were greater for the CAM (110 min [40-264]; and 9% [0-34], respectively) compared to a standard Holter (30 min [18-270]; and 0.3% [0-9], respectively). The total number of beats (P=0.017) and maximum (P=0.02) and mean (P=0.037) heart rates were lower for the CAM (113,806 ± 23,619 beats; 227 ± 35 bpm; and 88 ± 22 bpm, respectively) compared to the standard Holter (131,640 ± 40,037 beats; 260 ± 64 bpm; and 92 ± 26 bpm, respectively). The minimal heart rate (P=0.725), number of pauses (P=0.078), duration of the longest pause (P=0.087), number of ventricular ectopic complexes (P=0.55), ventricular couplets (P=0.186), ventricular triplets (P=0.203), ventricular tachycardia (P=0.05), Lown grade (P=0.233), presence or absence of ventricular bigeminy, trigeminy, supraventricular tachycardia, and atrial fibrillation (P=0.98) did not differ. The CAM missed some relevant events, like complex ventricular arrhythmias, and the Lown grade did not match in 5/19 dogs when comparing the devices. CONCLUSIONS: Cardiac Ambulatory Monitor can be used to record ECG traces in dogs over a prolonged period, allowing to detect arrhythmias. Due to some clinically relevant limitations, including a higher percentage of artefacts, a longer reading time (which precludes quantitative counts of >300ventricular premature complexes), and underestimation of complex ventricular arrhythmias, the CAM appears not suitable for quantitative arrhythmia analysis in dogs.

Feasibility of electroanatomic mapping and radiofrequency catheter ablation in Boxer dogs with symptomatic ventricular tachycardia.

BACKGROUND: Treatment for Boxers with ventricular tachycardia (VT) is limited. Electroanatomic mapping (EAM) facilitates identification of arrhythmogenic substrate for radiofrequency catheter ablation (RFCA). OBJECTIVE: Describe the use of EAM to guide RFCA in Boxers with VT. ANIMALS: Five client-owned Boxers with symptomatic VT or persistent VT despite antiarrhythmic medications. METHODS: Case series evaluating clinical, EAM, and before and after RFCA Holter data. RESULTS: Sustained VT was inducible in 3 dogs, but required aggressive stimulation protocols. Low-voltage areas consistent with electroanatomic scar were found in 2 dogs, located at the right ventricular (RV) outflow tract and cranial RV. Two dogs had a focal activation pattern of VT and 1 dog had a reentrant mechanism. After RFCA, all dogs no longer collapsed and had fewer runs of VT, 3 of which had 0 runs of VT. Number of ventricular premature beats increased in 3 dogs and decreased in 2 dogs, 1 of which had nearly complete resolution of all arrhythmias. Procedural complications included ventricular fibrillation (n = 2) with successful defibrillation, bruising or hemorrhage at the vascular access site (n = 4), retroperitoneal hemorrhage (n = 1), aortic and mitral regurgitation (n = 1), onset of frequent supraventricular tachycardia (n = 1), and persistent right pelvic limb lameness (n = 1). CONCLUSIONS AND CLINICAL IMPORTANCE: Electroanatomic mapping and RFCA are feasible in Boxers with VT. Based on this small cohort, RFCA may help decrease runs of VT and improve clinical signs. The anatomic substrate and electrophysiologic mechanisms are variable and require further study.

Three-dimensional electroanatomic mapping and radiofrequency catheter ablation of ventricular arrhythmia in a dog without structural heart disease.

A 1.5-year-old, female-spayed mix-breed dog was presented with recurrent episodes of shaking and excessive panting attributed to drug-refractory ventricular arrhythmia (VA) characterized predominantly by incessant periods of ventricular bigeminy. The VA had a narrow QRS morphology, suggestive of an origin near the His bundle or fascicular system. Diagnostic evaluation found no structural heart disease or underlying etiology. Three-dimensional electroanatomic mapping and radiofrequency catheter ablation were pursued. Voltage mapping demonstrated normal bi-ventricular voltage (≥1.5 mV) without any fractionated or multicomponent electrograms, indicating the absence of ventricular myocardial scar. Pace mapping identified an endocardial origin of the VA at the basal anterior septum of the left ventricle, distal to the His bundle and near the left bundle branch. Two ablation lesions were delivered to this site, and a left bundle branch block was temporarily induced. The dog recovered uneventfully. One month later, the owners reported a remarkable improvement in clinical signs, and follow-up 48-h Holter monitor found complete resolution of VA.

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.

Successful management of ventricular fibrillation and ventricular tachycardia using defibrillation and intravenous amiodarone therapy in a cat.

OBJECTIVE: To describe the successful management of ventricular fibrillation (VF) and ventricular tachycardia (VT) using cardiopulmonary resuscitation, including defibrillation, followed by continuous rate infusion of IV amiodarone, in a cat with cardiac arrest secondary to tachyarrhythmia. CASE SUMMARY: A 12-year-old previously healthy neutered male Scottish Fold cat presented following an acute episode of collapse. Initial physical examination revealed severe tachycardia and cardiovascular collapse. Within a few minutes after arrival, the cat experienced cardiopulmonary arrest. Electrocardiographic assessment was suggestive of VF, and CPR was initiated, including 2 rounds of defibrillation (2 joule/kg each), resulting in return of spontaneous circulation with sustained VT. After procainamide and lidocaine failed to result in conversion to normal sinus rhythm (NSR), continuous IV amiodarone therapy was initiated, and NSR was achieved. Echocardiography demonstrated severe systolic dysfunction, and tachycardia-induced cardiomyopathy (TICM) secondary to chronic VT was suspected; however, dilated cardiomyopathy (DCM) or end-stage hypertrophic cardiomyopathy could not be ruled out. The patient was discharged the following day with oral amiodarone and pimobendan. During a recheck examination performed 7 months later the cat was in NSR, with no direct evidence of long-term amiodarone adverse effects. The cat died acutely at home 8 months after discharge. NEW OR UNIQUE INFORMATION PROVIDED: This report is the first to describe the successful use of IV amiodarone in a cat to manage sustained VT following CPR.

Comparison of single- versus seven-day Holter analysis for the identification of dilated cardiomyopathy predictive criteria in apparently healthy Doberman Pinscher dogs.

INTRODUCTION: The primary objective of this study was to test whether seven-day Holter recording improves the sensitivity of detecting dilated cardiomyopathy (DCM) predictive criteria (DCMp) compared with 24-h Holter recording in asymptomatic Doberman Pinscher (DP) dogs. ANIMALS: Twenty-eight asymptomatic DP dogs with normal echocardiographic examinations. METHODS: Dogs with normal echocardiographic examinations underwent seven-day Holter monitoring. The presence of ≥50 ventricular premature complexes and or ≥ one couplet/one triplet/one episode of ventricular tachycardia per 24-h period was considered positive for DCMp. RESULTS: Five dogs were positive on the first day, and an additional six dogs tested positive from day two to seven of the Holter recording. The number of dogs positive for DCMp detected by four days was significantly different (p = 0.031) compared with the first-day Holter recording. CONCLUSIONS: Seven-day Holter recording detected significantly more dogs with DCMp compared with the first-day Holter recording. Follow-up studies are warranted to evaluate the long-term accuracy of multiple-day Holter analysis in predicting the development of DCM in DP dogs.

Heart rhythm during episodes of collapse in boxers with frequent or complex ventricular ectopy.

OBJECTIVES: To describe heart rhythm during collapse events in boxer dogs using ambulatory electrocardiogram and determine the predictive value of frequent or complex ventricular ectopy for collapse associated with ventricular tachycardia. MATERIALS AND METHODS: A total of 659 ambulatory electrocardiogram recordings from 429 boxer dogs were identified from a database in the UK. Summary statistics described the frequency and complexity of ventricular ectopy during all recordings, recordings in which collapse occurred and associated boxer demographics. Positive predictive values were calculated to investigate whether frequent ventricular ectopy was useful to predict heart rhythm during episodes of collapse. RESULTS: Of the 659 ambulatory electrocardiogram recordings, 250 recordings showed <50 single ventricular beats (Group 1), and frequent (≥50) or complex ventricular ectopy were observed in 409 recordings (Group 2). A total of 90 collapse events were observed in 72 ambulatory electrocardiograms from 68 dogs, comprising 30 dogs in Group 1 and 38 dogs in Group 2. In both groups, sinus rhythm was the most frequent collapse rhythm, followed by neurally mediated collapse and then ventricular tachycardia. The proportion of dogs that displayed ventricular tachycardia-associated episodic collapse given that they had frequent (≥50) or complex ventricular ectopy in the study population was 0.11 [95% confidence interval = 0.01 to 0.21]. CLINICAL SIGNIFICANCE: These results challenge the preconception that UK boxer dogs with collapse will have ventricular tachycardia and, consequently, the authors recommend definitive diagnosis of the cause of episodic collapse to guide selection of therapeutic drugs.

A QIL1 Variant Associated with Ventricular Arrhythmias and Sudden Cardiac Death in the Juvenile Rhodesian Ridgeback Dog.

The QIl1 gene produces a component of the Mitochondrial Contact Site and Cristae Organizing System that forms and stabilizes mitochondrial cristae junctions and is important in cellular energy production. We previously reported a family of Rhodesian Ridgebacks with cardiac arrhythmias and sudden cardiac death. Here, we performed whole genome sequencing on a trio from the family. Variant calling was performed using a standardized bioinformatics approach. Variants were filtered against variants from 247 dogs of 43 different breeds. High impact variants were validated against additional affected and unaffected dogs. A single missense G/A variant in the QIL1 gene was associated with the cardiac arrhythmia (p < 0.0001). The variant was predicted to change the amino acid from conserved Glycine to Serine and to be deleterious. Ultrastructural analysis of the biceps femoris muscle from an affected dog revealed hyperplastic mitochondria, cristae rearrangement, electron dense inclusions and lipid bodies. We identified a variant in the Q1l1 gene resulting in a mitochondrial cardiomyopathy characterized by cristae abnormalities and cardiac arrhythmias in a canine model. This natural animal model of mitochondrial cardiomyopathy provides a large animal model with which to study the development and progression of disease as well as genotypic phenotypic relationships.

Clinical safety of percutaneous ultrasound-guided fine-needle aspiration of adrenal gland lesions in 19 dogs.

OBJECTIVE: To evaluate the safety of fine-needle aspiration of adrenal gland lesions in dogs and to characterise the risks in a subset of patients with cytologically or histopathologically diagnosed phaeochromocytoma. MATERIALS AND METHODS: Retrospective review of medical records of dogs that underwent percutaneous ultrasound-guided fine-needle aspiration of adrenal gland lesions between August 2014 and December 2016. Nineteen dogs were identified, with three undergoing bilateral adrenal gland aspiration and one dog undergoing aspiration twice, yielding 23 cytology samples in total. Data collected included signalment, concurrent medical conditions, current medications, blood pressure and heart rate before adrenal fine-needle aspiration, imaging characteristics of the adrenal gland lesions and any clinically apparent procedure-related complications. RESULTS: Phaeochromocytoma was diagnosed in nine of 19 dogs, including one dog with bilateral phaeochromocytoma. One dog developed ventricular tachycardia following aspiration of an adrenal gland lesion cytologically consistent with a phaeochromocytoma. CLINICAL SIGNIFICANCE: Percutaneous ultrasound-guided fine-needle aspiration of adrenal gland lesions appears to be relatively safe, even in phaeochromocytoma, but further data are required to lend more weight to this finding. Minimally invasive aspirates could be considered as part of the diagnostic algorithm in the investigation of an incidentally detected adrenal gland lesion of uncertain clinical significance.

Ambulatory electrocardiographic evaluation of the occurrence of arrhythmias in healthy Salukis.

OBJECTIVE To determine the frequency and complexity of ventricular arrhythmias in a group of healthy Salukis evaluated by means of continuous Holter monitoring for 7 days. DESIGN Prospective case series. ANIMALS 25 healthy Salukis > 18 months old. PROCEDURES In all dogs, a history was obtained and a physical examination and transthoracic echocardiography were performed to verify the absence of structural cardiac disease. Dogs then underwent Holter monitoring for 7 days. Data recorded included heart rate parameters and the occurrence of conduction disturbances, ventricular premature complexes, ventricular couplets, ventricular triplets, ventricular bigeminy, ventricular trigeminy, and ventricular tachycardia. RESULTS 25 dogs (13 sexually intact females, 2 spayed females, and 10 sexually intact males) were enrolled in the study. All 25 dogs had at least one 24-hour period during which ventricular premature complexes were detected. Median number of ventricular premature complexes during any 24-hour period in all dogs was 2 (interquartile [25th to 75th percentile] range, 0 to 4). There were no significant differences between males and females in regard to median number of ventricular premature complexes per 24-hour period or recorded heart rate parameters. CONCLUSIONS AND CLINICAL RELEVANCE For Salukis in the study population, 7-day Holter monitoring revealed infrequent ventricular arrhythmias. These findings suggested that detection of a ventricular arrhythmia in a healthy Saluki may be an indication for further diagnostic evaluation.

Sudden cardiac death in a dog during Holter recording-R on T phenomenon.

A 6-year-old castrated male Golden Retriever was diagnosed with severe subaortic stenosis with severe left atrial enlargement and high heart rate due to atrial fibrillation. Treatment with digoxin and diltiazem to control ventricular response rate was initiated. Ambulatory electrocardiographic monitoring (Holter monitoring) was performed at the beginning of treatment and was repeated to evaluate the patient's response to drug therapy. Drug dose adjustments were made based on response to therapy as assessed by Holter monitoring. The dog experienced sudden death at home 19 days after beginning treatment while wearing the Holter monitor. Analysis of the Holter recording revealed marked increase in number and complexity of ventricular arrhythmias. A ventricular premature complex occurring on a T wave (R on T) was noted preceding the polymorphic ventricular tachycardia. This arrhythmia immediately degenerated into ventricular fibrillation followed by asystole. This case report describes the arrhythmia that preceded cardiac arrest and reviews the risk factors that could have potentiated the fatal arrhythmia in this dog.

Arrhythmogenic right ventricular cardiomyopathy in Boxer dogs: the diagnosis as a link to the human disease.

BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a myocardial disease with an increased risk for ventricular arrhythmias. The condition, which occurs in Boxer dogs, shares phenotypic features with the human disease arrhythmogenic cardiomyopathy (ACM) suggesting its potential as a natural animal model. However, there are currently no universally accepted clinical criteria to diagnose ARVC in Boxer dogs. We aimed to identify diagnostic criteria for ARVC in Boxer dogs defining a more uniform and consistent phenotype. METHODS AND RESULTS: Clinical records from 264 Boxer dogs from a referral veterinary hospital were retrospectively analysed. ARVC was initially diagnosed according to the number of ventricular premature complexes (VPCs) in the 24-hour-Holter-ECG in the absence of another obvious cause. Dogs diagnosed this way had more VPCs, polymorphic VPCs, couplets, triplets, VTs and R-on-T-phenomenon and syncope, decreased right ventricular function and dilatation in comparison to a control group of all other Boxer dogs seen by the Cardiology Service over the same period. Presence of couplets and R-on-T-phenomenon on a 24h-ECG were identified as independent predictors of the diagnosis. A diagnosis based on ≥100 VPCs in 24 hours, presence of couplets and R-on-T phenomenon on a 24h-ECG was able to select Boxer dogs with a phenotype most similar to human ACM. CONCLUSION: We suggest the diagnosis of ARVC in Boxer dogs requires two out of the three following criteria: presence of ≥ 100 VPCs, presence of couplets or R-on-T-phenomenon on a 24 h-ECG. This results in a uniform phenotype similar to that described in human ACM and may result in the adoption of the term ACM for this analogous condition in Boxer dogs.

Pyloric obstruction secondary to epicardial pacemaker implantation: a case report.

A 10-year old Lhasa Apso dog was presented for an acute history of exercise intolerance and hind limb weakness. High grade second degree atrioventricular block with an atrial rate of 200 beats per minute, ventricular rate of 40 beats per minute and an intermittent ventricular escape rhythm, was diagnosed on electrocardiograph. A transdiaphragmatic, unipolar, epicardial pacemaker was implanted without immediate surgical complications. Severe vomiting was noted 12 h post-operatively. Abdominal ultrasound and a barium study supported a diagnosis of pyloric outflow obstruction and exploratory abdominal surgery was performed. The pyloric outflow tract appeared normal and no other causes of an outflow obstruction were identified. The epicardial generator was repositioned from the right to the left abdominal wall. Pyloric cell pacing was presumed to be the cause for the pyloric obstruction and severe vomiting, and this was thought to be due to close proximity of the pacemaker generator to the pylorus situated in the right abdominal wall. Repositioning of the pulse generator to the left abdominal wall resulted in resolution of vomiting.

Valor prognóstico da variabilidade da frequência cardíaca e da eletrocardiografia ambulatorial em cães Boxer com cardiomiopatia arritmogênica do ventrículo direito / Prognostic value of heart rate variability and Holter monitoring in Boxer dogs with arrhythmogenic right ventricular cardiomyopathy

A cardiomiopatia arritmogênica do ventrículo direito (CAVD) é uma importante causa de morte súbita em cães da raça Boxer. A validação de fatores prognósticos para essa doença auxiliaria na detecção de animais mais gravemente afetados e sua exclusão dos programas de reprodução. O objetivo deste estudo foi avaliar o valor prognóstico da presença de manifestações clínicas, dos índices de variabilidade de frequência cardíaca (VFC) e das arritmias supraventriculares ou ventriculares registradas à monitorização eletrocardiográfica com Holter na sobrevida de cães Boxer em diferentes estágios da CAVD. Essas variáveis foram analisadas, de forma prospectiva, em 69 cães Boxer, divididos em cinco grupos: cães Boxer controle (grupo CB, <50 VPC/24 horas, n=28), cães Boxer suspeitos (grupo SB, 50 a 300 VPC/24 horas, n=8), cães Boxer com CAVD (grupo ARVC, >300 VPC/24 horas, n=19), cães Boxer com CAVD e disfunção sistólica sem insuficiência cardíaca congestiva (grupo SDB sem ICC, n=6) e com ICC (grupo SDB com ICC, n=8). A análise estatística compreendeu teste ANOVA, correlação de Pearson e análise de riscos proporcionais de Cox. Comparando-se com o grupo CB, não foi encontrada diminuição nos índices de VFC nos grupos SB, ARVC ou SDB sem ICC; por outro lado, o grupo SDB com ICC apresentou diminuição desses índices. Não houve relação entre os índices de VFC e a morte de origem cardíaca; porém, a presença de síncopes com ou sem sinais clínicos de ICC e o número de episódios de taquicardia ventricular (TV) correlacionaram-se com a sobrevida dos animais. Estes resultados permitem concluir que a presença de sinais clínicos de ICC, a presença de síncopes e o número de TV ao Holter apresentam valor prognóstico de sobrevida em cães Boxer com CAVD.(AU)

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an important cause of sudden death in Boxer dogs. Validation of prognostic factors for this disease could help in detecting more severely affected animals and their exclusion from breeding programs. The aims of this study were to evaluate the prognostic significance of presence of symptoms, heart rate variability (HRV) indices and ventricular or supraventricular arrhythmias recorded by Holter monitoring on survival of Boxer dogs with ARVC at different stages. Symptoms, arrhythmias registered on Holter and five HRV indices were prospectively analyzed in 69 client-owned Boxer dogs divided into five groups: control Boxer dogs (CB group, <50 VPC/24 hours, n=28), suspicious Boxers (SB group, 50 to 300 VPC/24 hours, n=8), Boxers with ARVC (ARVC group, >300 VPC/24 hours, n=19), Boxers with ARVC and systolic dysfunction without congestive heart failure (SDB without CHF group, n=6) and with CHF (SDB with CHF group, n=8). Statistical analyses consisted of an ANOVA test, Pearson correlation and Cox's proportional hazards regression. Compared to the CB group, no decrease in HRV indices was found in SB, ARVCB or SDB without CHF groups; otherwise, SDB with CHF group had impaired indices. No relation was found between HRV indices and cardiac-related death, but the presence of syncopes with or without clinical signs of heart failure and number of ventricular tachycardia (VT), were correlated with survival. These results allow us to conclude that the presence of symptoms of heart failure, presence of syncopes and number of VT on Holter examination seem to have prognostic value in Boxer ARVC.(AU)

Polymorphism identification and cardiac gene expression analysis of the calsequestrin 2 gene in broiler chickens with sudden death syndrome.

Sudden death syndrome (SDS) in broilers is a cardiac disease associated with ventricular tachycardia (VT) and ventricular fibrillation (VF); however, its pathogenesis at the molecular level is not precisely determined. Downregulation and mutations of calsequestrin 2 (CASQ2), a major intracellular Ca(2+) buffer, have been associated with VT and sudden cardiac death (SCD) in humans but in chickens there is no report describing CASQ2 abnormalities in cardiac diseases. In order to better understand the molecular mechanisms predisposing the myocardium to fatal arrhythmia in broilers, the mRNA expression level of chicken CASQ2 gene (chCASQ2) in the left ventricle of dead broilers with SDS was determined and compared to healthy broilers using quantitative real-time PCR (qPCR). To determine the probable mutations in chCASQ2, PCR and direct sequencing were also done. Results showed a reduction in chCASQ2 expression in broilers dead by SDS. Three novel mutations (K289R, P308S, D310H) which are absent in healthy broilers were observed in chCASQ2. It is concluded that susceptibility to fatal cardiac arrhythmia in SDS may be associated with changes in intracellular Ca(2+) balance due to mutation and downregulation of chCASQ2.

Time-domain signal-averaged electrocardiogram in healthy German Shepherd and Boxer dogs / Eletrocardiograma de alta resolução (ECGAR) no domínio do tempo em cães sadios das raças Pastor Alemão e Boxer

Signal-averaged electrocardiogram (SAECG) identifies ventricular late potentials (LP), low-amplitude electrical signals that are markers of slow cardiac conduction in fibrous myocardium, consisting in a predictive factor for sudden death in dogs at risk of sustained ventricular tachycardia. The aim of this study was to establish reference values of SAECG for German Shepherd and Boxer dogs. SAECG was performed in 19 German Shepherd and 28 Boxer client-owned dogs, and parameters analyzed were QRSd (duration of filtered QRS), LAS<40μV (duration of low-amplitude signals in terminal portion of filtered QRS) and RMS40 (root square of mean voltage over the last 40 milliseconds of filtered QRS), with two different filters (25-250 Hz and 40-250 Hz). Statistical analyses was achieved by T Student test (p<0.05) to identify differences between the two groups and between the values obtained with the two filters. No statistical difference was found in SAECG variables between the two breeds with the two different filters (p>0.05). Achieving normal values of SAECG in German Shepherd and Boxer dogs is important to further research late potentials in animals of these breeds with hereditary ventricular tachycardia or arrhythmogenic cardiomyopathy and identification of individuals at high risk of cardiac-related sudden death...

O eletrocardiograma de alta resolução (ECGAR) identifica os potenciais tardios (PT), sinais elétricos de baixa amplitude considerados marcadores de condução cardíaca lenta de áreas fibrosadas do miocárdio, cuja presença consiste em fator preditivo de morte súbita em cães com taquicardia ventricular sustentada. O objetivo deste estudo foi o estabelecimento de valores de referência para o ECGAR de cães Boxer (n=28) e Pastor Alemão (n=19). Os seguintes parâmetros do ECGAR foram analisados: dQRS (duração do QRS filtrado), LAS<40μV (duração dos sinais de baixa amplitude no final do QRS filtrado) e RMS40 (raiz quadrada da voltagem média do final do QRS filtrado), com dois tipos diferentes de filtro (25-250 Hz e 40-250 Hz). Análise estatística foi realizada por meio do teste T de Student (p<0,05) para identificar diferenças entre os dois grupos e entre os valores obtidos com os dois filtros. Não foram encontradas diferenças significativas entre as variáveis de ECGAR nas duas raças estudadas com os dois diferentes filtros (p>0,05). A obtenção dos valores de normalidade de ECGAR em cães dessas raças auxiliará na realização de futuras pesquisas de potenciais tardios em animais com taquicardia ventricular hereditária ou cardiomiopatia arritmogênica, bem como na identificação dos indivíduos com alto risco de morte súbita de origem cardíaca...

Effect of short-term rapid ventricular pacing followed by pacing interruption on arterial blood pressure in healthy pigs and pigs with tachycardiomyopathy.

Ventricular tachycardia may lead to haemodynamic deterioration and, in the case of long term persistence, is associated with the development of tachycardiomyopathy. The effect of ventricular tachycardia on haemodynamics in individuals with tachycardiomyopathy, but being in sinus rhythm has not been studied. Rapid ventricular pacing is a model of ventricular tachycardia. The aim of this study was to determine the effect of rapid ventricular pacing on blood pressure in healthy animals and those with tachycardiomyopathy. A total of 66 animals were studied: 32 in the control group and 34 in the study group. The results of two groups of examinations were compared: the first performed in healthy animals (133 examinations) and the second performed in animals paced for at least one month (77 examinations). Blood pressure measurements were taken during chronic pacing--20 min after onset of general anaesthesia, in baseline conditions (20 min after pacing cessation or 20 min after onset of general anaesthesia in healthy animals) and immediately after short-term rapid pacing. In baseline conditions significantly higher systolic and diastolic blood pressure was found in healthy animals than in those with tachycardiomyopathy. During an event of rapid ventricular pacing, a significant decrease in systolic and diastolic blood pressure was found in both groups of animals. In the group of chronically paced animals the blood pressure was lower just after restarting ventricular pacing than during chronic pacing. Cardiovascular adaptation to ventricular tachycardia develops with the length of its duration. Relapse of ventricular tachycardia leads to a blood pressure decrease more pronounced than during chronic ventricular pacing.