Myocardial infarction secondary to a disseminated coagulopathy in a cow

A 3-year-old Holstein cow was presented with a history of high fever, jaundice and subsequent recumbency. The animal died 3 hours after arrival at our department; continuous electrocardiographic examination was performed during those last 3 hours. There were ventricular premature beats (VPBs) with high frequency and complex patterns (bigeminal, trigeminal, repetitive or early cycle VPBs) and paroxysms of ventricular tachycardia (VT). Serum CK-MB was markedly elevated. On histopathological examination, large areas of myocardial necrosis were found in the anterior aspects of the left ventricle. Large, partially organized thrombi occluded the intramural coronary arteries within and adjacent to the lesion. From the histopathological findings, it appeared that a disseminated coagulopathy caused the thromboembolism in the intramural coronary arteries, resulting in acute myocardial infarction (AMI). Various clinical findings, such as arrhythmias, were similar to those in man.     

Orthodromic atrioventricular reciprocating tachycardia conducted with intraventricular conduction disturbance mimicking ventricular tachycardia in an English Bulldog

Electrocardiographic tracings of an English Bulldog referred for cardiogenic shock due to an orthodromic atrioventricular reciprocating tachycardia conducted with intraventricular conduction disturbance and mimicking ventricular tachycardia (VT) are presented. At admission the surface ECG showed a wide QRS complex tachycardia (WCT) that was converted to sinus rhythm using manual cardioversion (chest thump). This change revealed pre-existing right bundle branch block, and a final diagnosis of supraventricular tachycardia (SVT) with intraventricular conduction disturbance was made. Electrophysiologic study defined the SVT mechanism as an atrioventricular macroreentrant tachycardia mediated by a single mid-septal accessory pathway. The differentiation between various types of WCT is essential when antiarrhythmic therapy is considered. The surface ECG should be systematically evaluated in order to recognize the characteristic features of SVT and VT. Moreover chest thump procedure can be very helpful in the attempt to convert the rhythm to sinus rhythm and to correctly recognize the underlying arrhythmia.     

Treatment of sustained monomorphic narrow‐complex ventricular tachycardia in a 16‐year‐old Arab mare with a constant rate of infusion of lidocaine and oral propranolol

A 16‐year‐old Arab mare was referred for treatment of a tachydysrhythmia detected on electrocardiogram by the referring veterinarian. Monomorphic, narrow‐complex ventricular tachycardia (VT) was confirmed by electro‐cardiogram in a normal base‐apex configuration. Subsequent diagnostic testing, including echocardiography and measurement of plasma cardiac troponin concentration, did not reveal a definitive cause for the dysrhythmia. Conversion of VT to ventricular bigeminy occurred following treatment with magnesium sulfate and lidocaine hydrochloride, administered intravenously. Treatment with orally administered propranolol subsequently led to conversion to sinus rhythm with intermittent ventricular premature complexes (VPCs). Oral prednisolone treatment was also initiated to address the possibility that VT resulted from underlying myocarditis. The mare was discharged with oral propranolol, a tapering course of prednisolone, and exercise restriction. Follow‐up cardiac examination 6 weeks later revealed persistent, intermittent VPCs and reversion to VT occurred during exercise. Sinus rhythm with intermittent VPCs was re‐established following the administration of lidocaine. The mare was again discharged with oral propranolol therapy, which was subsequently replaced with oral sotalol. Sudden death occurred 4 weeks later but a post mortem examination was not performed.     

Ventricular tachycardia in English bulldogs with localised right ventricular outflow tract enlargement

Objectives : To describe the electrocardiographic characteristics of ventricular tachycardia arising from the right ventricular outflow tract and the particular association between this arrhythmia and the presence of localised right ventricular outflow tract enlargement in English bulldogs. Methods : Five English bulldogs were referred with a history of syncope or cardiogenic shock. In all dogs, 12‐lead surface ECG, thoracic radiograph and echocardiography were collected. In all but one dog 24‐hours Holter monitoring and signal‐averaged ECGs was examined and in one dog electrophysiological study and radiofrequency catheter ablation of the VT substrate was performed. Results : Documented arrhythmias included a single sustained monomorphic wide QRS tachycardia in four dogs, and an alternans of two different monomorphic forms in one dog. Mean QRS duration during tachy‐cardia was 91·6 ±9·83 milliseconds. QRS complexes manifested a left bundle branch block morphology and an inferior axis (81 ±13·73°). R wave notching was present in the caudal (inferior) leads in three tachy‐cardias. Lead I was negative in 3 of 6, positive in 1 of 6 and isodiphasic in 2 of 6. Lead aVL was negative in 5 of 6 and positive in 1 of 6. Signal‐averaged electrocardiograms revealed late potentials in three dogs. Echocardiography showed a localised right ventricular outflow tract enlargement in all dogs. Cardiac map‐ping established two sites of origin of ventricular tachycardia within the right ventricular outflow tract in one dog: caudal free‐wall and cranial‐septal. Clinical Significance : The presence of a localised right ventricular outflow tract enlargement and ventricular tachycardia with left bundle branch block morphology could suggest segmental arrhythmogenic right ven‐tricular cardiomyopathy in the English bulldog.     

Phenytoin sodium as a treatment for ventricular dysrhythmia in horses

Five adult horses with ventricular extra systoles (VES) and 2 with ventricular tachycardia (VT) refractory to treatment with rest, anti-inflammatory drugs, lidocaine, or procainamide were treated with phenytoin sodium p.o. q12h. The starting dosage of phenytoin was 20 or 22 mg/kg body weight (BW) q12h, and the maintenance dosage varied from 8 to 17 mg/kg BW q12h. The mean +/- standard deviation therapeutic blood concentration of total phenytoin was 8.8 +/- 2.1 mg/L, and the mean concentration of free phenytoin of 2.5 +/- 0.5 mg/L was relatively constant at a range of 24 to 29% of the total phenytoin concentration. In all horses, both VES and VT were abolished after treatment with phenytoin. On the basis of the results of this clinical study, the authors propose an initial dose of 20 mg/kg BW q12h for the first 3 or 4 dosages, followed by a maintenance dose of 10 to 15 mg/kg BW q12h. Phenytoin plasma concentrations should be monitored during therapy. High plasma concentrations were associated with adverse effects such as recumbency and excitement. In this study, which included a limited number of diverse patients, phenytoin sodium appeared to be an inexpensive and effective treatment for persistent VES or VT in cases where conventional treatment had failed.     

Bradycardia-associated syncope in 7 Boxers with ventricular tachycardia (2002-2005).

BACKGROUND: Syncope is a recognized problem in Boxers and often is the result of rapid ventricular tachycardia (VT). Affected dogs may have echocardiographic evidence of dilated cardiomyopathy, but frequently have normal echocardiograms. Although VT is probably the most common cause of syncope in Boxers, neurocardiogenic bradycardia can also occur. OBJECTIVE: We describe 7 Boxers with comorbid VT and neurocardiogenic bradycardia, wherein the syncope was secondary to bradycardia rather than VT. ANIMALS: Seven Boxers were selected from a larger population of Boxers with Holter-documented VT because these dogs had documented bradycardia at the time of syncope. METHODS: Retrospective study. RESULTS: Although all dogs had Holter-documented VT, the etiology of the syncopal episodes was consistent with neurocardiogenic bradycardia. CLINICAL IMPORTANCE: Neurocardiogenic bradycardia or VT can occur as isolated problems in Boxers. In some Boxers, VT and potential or manifest neurocardiogenic bradycardia coexist. The administration of a beta-blocker or sotalol to such dogs can aggravate or precipitate neurocardiogenic bradycardia-related syncope.     

Bradycardia-Associated Syncope in 7 Boxers with Ventricular Tachycardia (2002–2005)

Background: Syncope is a recognized problem in Boxers and often is the result of rapid ventricular tachycardia (VT). Affected dogs may have echocardiographic evidence of dilated cardiomyopathy, but frequently have normal echocardiograms. Although VT is probably the most common cause of syncope in Boxers, neurocardiogenic bradycardia can also occur.
Objective: We describe 7 Boxers with comorbid VT and neurocardiogenic bradycardia, wherein the syncope was secondary to bradycardia rather than VT.
Animals: Seven Boxers were selected from a larger population of Boxers with Holter-documented VT because these dogs had documented bradycardia at the time of syncope.
Methods: Retrospective study.
Results: Although all dogs had Holter-documented VT, the etiology of the syncopal episodes was consistent with neurocardiogenic bradycardia.
Clinical Importance: Neurocardiogenic bradycardia or VT can occur as isolated problems in Boxers. In some Boxers, VT and potential or manifest neurocardiogenic bradycardia coexist. The administration of a β-blocker or sotalol to such dogs can aggravate or precipitate neurocardiogenic bradycardia-related syncope.     

Transcatheter closure of congenital ventricular septal defects in 3 dogs with a detachable coil

The purpose of this study was to evaluate the feasibility, safety, and efficacy of transcatheter closure in dogs with a congenital perimembranous ventricular septal defect (VSD) by using a detachable coil. No dogs showed any symptoms, and results of chest X-rays and ECGs were normal. The diameters of VSD ranged from 2 to 4 mm on echocardiogram. The defect was 2-2.5 mm from the aortic valve. A detachable coil (size 5 mm with 5 loops) designed for patent ductus arteriosus was delivered via the transarterial route. The device was successfully employed in all dogs. A minimal residual shunt was observed in all dogs even though Qp/Qs decreased. Hemolysis and a rate-dependent right-bundle branch block were observed in 1 dog, but there was no clinical significance. No major complication was noted. Pathologic examination after 1 year revealed that the coils were covered with tissue without significant damage to the His-Purkinje conduction system. In conclusion, transcatheter closure of a small perimembranous VSD with a detachable coil can be achieved without major complications or significant pathologic damage at the lesion site.     

Genetic Analysis of Ventricular Arrhythmia in Young German Shepherd Dogs

Background: Ventricular arrhythmias (VA) and sudden death are inherited in German Shepherd Dogs (GSDs).
Objectives: To estimate the genetic parameters (heritabilities and correlations) of 3 traits of VA (single premature ventricular complexes (PVCs), 2 consecutive PVCs (couplets), and 3 or more consecutive PVCs—ventricular tachycardia [VT]).
Animals: Three hundred and ninety-eight GSDs.
Methods: Prospective, observational, case control study. Dogs were phenotyped by 24-hour ambulatory ECG from 6 to 45 weeks of age. Edited ECG records included the number of incidents of (1) single PVCs, (2) couplets, and (3) VT.
Results: A data set of 1,239 Holter records from 398 GSDs was used to estimate genetic variables. Phenotypic correlations for affectedness (binarily coded 0/1) of the 3 traits ranged from 0.55 to 0.74, whereas correlations for severity (continuous values of 24-hour VA counts) ranged from 0.26 to 0.39. Estimates of genetic correlation among the severity traits were 0.06 to 0.27. Estimated heritabilities were 0.54, 0.54, and 0.46 for affectedness and 0.33, 0.69, and 0.69 for severity of PVCs, couplets, and VT, respectively. Month and year of birth and age at ECG recording had significant effects on all 3 traits. Season of ECG recording had a significant effect on the number of single PVCs, but not couplets or incidents of VT. Age of onset differed, with single PVCs appearing an average of 4 days earlier than couplets and VT.
Conclusion: These results imply a strong genetic component for this disease but suggest that differences in the 3 traits should be taken into consideration in studies to identify the underlying genes.     

Arrhythmogenic right ventricular cardiomyopathy associated with severe left ventricular involvement in a cat

An 8-year-old, 4 kg, intact female, domestic shorthaired cat was referred for tachypnea and pleural effusion. A 24-h Holter recording showed numerous polymorphic ventricular premature complexes with left and right bundle branch block morphology. Echocardiographic examination revealed right atrial and ventricular dilation. The right ventricular free wall was thin and aneurysmal. The cat died 10 days after initiation of antiarrhythmic therapy. Gross and histopathological findings were consistent with arrhythmogenic right ventricular cardiomyopathy (ARVC) associated with severe left ventricular involvement.     

松针挥发油对乌头碱诱发大鼠心律失常的影响

为了测定松针挥发油对乌头碱诱发大鼠心律失常的影响,采用静脉注射乌头碱复制大鼠心律失常的动物模型,观察灌胃给药松针挥发油对抗乌头碱诱发大鼠心律失常的作用。结果发现,松针挥发油的低、中、高剂量可显著延迟VP(室性早博)和VT(室性心动过速)的出现(与阴性对照组对比P0.01、P0.05),而以中剂量效果最好(与阴性对照组对比P0.01)。阳性对照组普罗帕酮对VT(室性心动过速)和VF(心室纤颤)的出现具显著延迟作用(与阴性对照组对比P0.01),但对VP的出现与阴性对照组相比却无显著差别(P0.05)。说明松针挥发油对药物诱发的心律失常具对抗作用。     

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.     

Ventricular dyssynchrony as a cause of structural disease in the heart of Dorper sheep

Ventricular dyssynchrony is a disturbance of the normal, organized electromechanical coupling of the two ventricles. This condition has many causes, such as left bundle branch block, ventricular preexcitation, right ventricular pacing and right ventricular premature ventricular complexes (PVCs). Ventricular dyssynchrony has many adverse haemodynamic effects on the left ventricle and we wanted to know whether these adverse haemodynamic effects might have any structural consequences on the left ventricles of such hearts. Six healthy Dorper wethers were subjected to numerous right ventricular PVCs to induce ventricular dyssynchrony in order to determine whether any structural consequences will occur in the left ventricles of these hearts. Myocarditis in the musculature of the left ventricles of all six these hearts was seen.     

Failure of spectro-temporal mapping to detect ventricular late potentials in dogs

OBJECTIVE: To determine whether ventricular late potentials (LP) identified by time-domain analysis (TDA) of the signal-averaged ECG could be identified by three-dimensional frequency-domain analysis (FDA). ANIMALS: 11 dogs (9 of which subsequently died suddenly) with ventricular tachyarrhythmias (10 with ventricular tachycardia) and abnormal TDA of the signal-averaged ECG. PROCEDURE: Signal-averaged ECG that were abnormal when analyzed in the time domain subsequently were processed further in the frequency domain. Correlation ratios were calculated, and spectro-temporal maps were plotted, which were then compared with control data. RESULTS: Three-dimensional FDA did not detect LP. CONCLUSIONS AND CLINICAL RELEVANCE: LP may be detectable by TDA of the signal-averaged ECG and may be a specific marker for VT and sudden death in some dogs. However, FDA by use of the method applied in this study is invalid.     

Clinical, echocardiographic, and electrocardiographic abnormalities in Boxers with cardiomyopathy and left ventricular systolic dysfunction: 48 cases (1985-2003)

OBJECTIVE: To identify clinical, echocardiographic, and electrocardiographic abnormalities in Boxers with cardiomyopathy and echocardiographic evidence of left ventricular systolic dysfunction. DESIGN: Retrospective study. ANIMALS: 48 mature Boxers. PROCEDURE: Medical records were reviewed for information on age; sex; physical examination findings; and results of electrocardiography, 24-hour ambulatory electrocardiography, thoracic radiography, and echocardiography. RESULTS: Mean age of the dogs was 6 years (range, 1 to 11 years).Twenty (42%) dogs had a systolic murmur, and 9 (19%) had ascites. Congestive heart failure was diagnosed in 24 (50%) dogs. Seventeen (35%) dogs had a history of syncope. Mean fractional shortening was 14.4% (range, 1% to 23%). Mean left ventricular systolic and diastolic diameters were 4.5 cm (range, 3 to 6.3 cm) and 5.3 cm (range, 3.9 to 7.4 cm), respectively. Twenty-eight (58%) dogs had a sinus rhythm with ventricular premature complexes (VPCs), and 20 had supraventricular arrhythmias (15 with atrial fibrillation and 5 with sinus rhythm and atrial premature complexes). Sixteen of the dogs with supraventricular arrhythmias also had occasional VPCs. Morphology of the VPCs seen on lead II ECGs was consistent with left bundle branch block in 25 dogs, right bundle branch block in 8, and both in 11. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that Boxers with cardiomyopathy and left ventricular dysfunction frequently have arrhythmias of supraventricular or ventricular origin. Whether ventricular dysfunction was preceded by electrical disturbances could not be determined from these data, and the natural history of myocardial disease in Boxers requires further study.     

Arrhythmogenic right ventricular dysplasia/cardiomyopathy in a Siberian husky

A seven-month-old male Siberian husky was presented with a recent history of anorexia, hindlimb weakness and syncope. Physical examination revealed severe tachycardia, tachypnoea and dyspnoea. Mucous membranes were pale and femoral pulses were weak. An electrocardiogram showed sustained ventricular tachycardia with a left bundle branch block configuration. Thoracic radiographs revealed slight right ventricular enlargement and two-dimensional echocardiography revealed mild right ventricular dilation at the cardiac apex and some hyperechogenic areas on the right side of the interventricular septum. Administration of intravenous lignocaine converted the ventricular tachycardia to sinus rhythm. The maintenance antiarrhythmic therapy consisted of oral procainamide and propranolol. Three weeks later the dog died suddenly. On postmortem examination, the right ventricular free wall was very thin at the apex, infundibulum and caudal aspect of the right ventricular parietal wall, similar to the 'triangle of dysplasia' of human patients. Histopathological examination revealed replacement of several areas of right ventricular free wall myocardium with connective tissue and fat. The right atrium and left ventricle were less severely affected by the same lesions. The clinical and pathological findings are similar to those reported in young people with arrhythmogenic right ventricular dysplasia/cardiomyopathy.     

Arrhythmogenic right ventricular cardiomyopathy in a dog

An 8-month-old Labrador retriever bitch was evaluated for sudden-onset, progressive abdominal distension. Physical examination revealed an exaggerated inspiratory effort, severe ascites, bilateral jugular vein distension, and hypokinetic femoral arterial pulses. Thoracic auscultation detected tachycardia with muffled heart sounds, without audible cardiac murmurs. Thoracic radiographs identified severe right ventricular enlargement and pleural effusion. The electrocardiogram was consistent with incomplete right bundle branch block or right ventricular enlargement. Echocardiography demonstrated severe right ventricular and atrial dilation, secondary tricuspid regurgitation, and thinning and hypocontractility of the right ventricular myocardium. Left heart chamber sizes were slightly decreased, with normal left ventricular contractility. A diagnosis of arrhythmogenic right ventricular cardiomyopathy was reached, based on the characteristic clinical, electrocardiographic, radiographic and echocardiographic findings, and the exclusion of other causes of isolated right ventricular failure. Treatment effected good control of clinical signs, until acutely decompensated congestive right heart failure led to euthanasia after 4 months. Arrhythmogenic right ventricular cardiomyopathy is a well-described clinical entity in humans, and has previously been documented in 3 male dogs. The condition is characterised by progressive fibro-adipose replacement of right ventricular myocardium, while the left ventricle usually remains unaffected. It should be considered a differential diagnosis in any young dog presented with isolated right heart failure, syncope, or unexplained ventricular tachyarrhythmias. This article reports the 1st case of arrhythmogenic right ventricular cardiomyopathy in a female dog, and highlights its echocardiographic features.     

Guttural pouch empyema secondary to a periocular foreign body

This report describes a 3‐year‐old gelding presenting with signs of injury to its left eye following an accident in which the horse crashed into a hedge. The first treatment attempted to treat infections in the eye and respiratory tract due to secretions identified in the trachea. The horse did not improve and further clinical and radiographic evaluations detected a guttural pouch empyema. Surgical drainage was performed and antimicrobial treatment continued. However, the horse presented with severe epistaxis and euthanasia was elected due to suspected arterial rupture. At necropsy, a round and stiff branch plant was found creating a fistula from the left orbit to the left guttural pouch. Another branch was found inside the pouch, confirming the origin of the persistent infection and severity of the tissue lesion.     

不同温湿指数环境下奶牛阴道温度的变化规律

为探究不同温湿指数(THI)环境下奶牛阴道温度的变化规律,试验分别在高THI(78.5±3.2)、中THI(70.4±4.1)、低THI(56.3±5.5)环境下连续7d监测15头健康妊娠奶牛的阴道温度及所在牛舍内外的温度和相对湿度。结果表明:高THI环境下奶牛平均阴道温度、日极值均差、测期极值差极显著高于中、低THI环境下奶牛相应的测值(P<0.01);奶牛日平均阴道温度和日平均THI、日最高阴道温度和日受热时长的相关系数r分别是0.811、0.896(P<0.01);引起日平均阴道温度、日最高阴道温度开始快速升高的日平均THI、日最大THI分别为71.4、77.3,日受热时长为10.6h时日最高阴道温度变化出现拐点。由此可见,高THI环境下奶牛阴道温度变化幅度大;相比THI,日受热时长会影响奶牛阴道温度的变化。     

Treatment time,ease of use and cost associated with use of Equashield™, PhaSeal®, or no closed system transfer device for administration of cancer chemotherapy to a dog model

This prospective experimental simulation study evaluated the efficiency, ease of use (EOU) and cost of administering chemotherapy with two closed system transfer devices (CSTD, Equashield? and PhaSeal^®) and no CSTD. Forty‐six veterinary technicians (VT) working in oncology specialty practices were timed during chemotherapy administration simulated with water and a model canine limb 10 times with each system and with no CSTD. EOU and likelihood of recommending each system were rated by VT using visual analog scales. Costs were obtained from veterinary distributors. Administration was fastest with Equashield? (P = 0.0003), but the difference was not enough to affect case flow. Equashield? was easier to use than PhaSeal^® or no CSTD (P = 0.002), however VT recommended both CSTD more strongly than no CSTD (P < 0.0001). Equashield? cost less than PhaSeal^® but was sold only in bulk quantities. CSTD did not decrease efficiency in administering chemotherapy and were readily accepted by VT.