Cough-induced severe bradycardia and syncope in a dog.

A 10-year-old spayed female shih tzu dog was brought to the hospital because of recurring syncope that occurred simultaneously with a cough. Physical examination did not reveal an abnormal heart rhythm or abnormal heart sounds. Electrocardiography revealed sinus arrest of 4.7 s with intermittent escape beats during coughing. Additional examinations, including thoracic radiography, clinical pathology, and echocardiography, revealed no abnormalities of concern. Forty-eight-hour Holter monitoring captured 1 syncopal episode following severe coughing, during which the longest sinus arrest lasted 16 s with intermittent escape beats. This observation confirmed our strong suspicion that coughing was the cause of varying degrees of sinus arrest in this dog. Theophylline, codeine, and short-term prednisolone were prescribed to treat the dog's cough. The daily episodes of syncope ceased and coughing decreased. Subsequent 48-hour Holter monitoring revealed no abnormal pauses, and the owner did not report syncope. Theophylline and codeine were continued for 5 mo, during which time no syncope occurred. To our knowledge, this case provides the first clear evidence of a correlation between cough-induced sinus arrest and syncope in a veterinary patient, as confirmed by Holter monitoring and electrocardiography. Key clinical message: Cough-induced severe bradycardia and syncope were identified in a shih tzu dog. After the antitussive medication was adjusted, the signs resolved.

Bradycardie sévère et syncope provoquées par la toux chez un chienUne chienne shih tzu stérilisée âgée de 10 ans a été amenée à l'hôpital en raison d'une syncope récurrente survenue simultanément avec une toux. L'examen physique n'a révélé aucun rythme cardiaque anormal ni bruits cardiaques anormaux. L'électrocardiographie a révélé un arrêt sinusal de 4,7 s avec des battements d'échappements intermittents lors de la toux. Des examens complémentaires, notamment une radiographie thoracique, des analyses en pathologie clinique et une échocardiographie, n'ont révélé aucune anomalie préoccupante. Une surveillance Holter de 48 heures a capturé 1 épisode syncopal à la suite d'une toux sévère, au cours duquel l'arrêt sinusal le plus long a duré 16 s avec des battements d'échappements intermittents. Cette observation a confirmé nos fortes suspicions selon lesquelles la toux était la cause de divers degrés d'arrêt sinusal chez ce chien. De la théophylline, de la codéine et de la prednisolone de courte durée ont été prescrites pour traiter la toux du chien. Les épisodes quotidiens de syncope ont cessé et la toux a diminué. Une surveillance Holter ultérieure de 48 heures n'a révélé aucune pause anormale et le propriétaire n'a pas signalé de syncope. La théophylline et la codéine ont été poursuivies pendant 5 mois, période pendant laquelle aucune syncope ne s'est produite. À notre connaissance, ce cas constitue la première preuve claire d'une corrélation entre l'arrêt sinusal induit par la toux et la syncope chez un patient vétérinaire, comme le confirme la surveillance Holter et l'électrocardiographie.Message clinique clé :Une bradycardie et une syncope sévères induites par la toux ont été identifiées chez un chien shih tzu. Après ajustement du traitement antitussif, les signes ont disparu.(Traduit par Dr Serge Messier).

ECHOCARDIOGRAPHY IN THIRTY AMERICAN FLAMINGOS (PHOENICOPTERUS RUBER) AND A CASE OF SUSPECTED NEURALLY MEDIATED REFLEX SYNCOPE.

Heart disease in birds contributes to premature death and is usually detected postmortem. Echocardiography is a sensitive and noninvasive diagnostic modality but reported standard values for many species of birds, including American flamingos (Phoenicopterus ruber), are unavailable. Echocardiography was opportunistically performed on 30 unsedated American flamingos during their annual routine health examination. Structural heart disease was not found in any of the examined birds. However, 18 birds showed varying degrees of dynamic intraventricular obstruction. Echocardiographic parameters are reported. Benign neurocardiogenic weakness or syncopal events during handling were suspected in three birds. Stress combined with an intraventricular obstruction is believed to have triggered a cascade of parasympathetic innervation and sympathetic inhibition, similar to neurally mediated reflex syncope in humans.

Hypertrophic cardiomyopathy in a dog: a systematic diagnostic approach.

A seven-year-old female neutered Parson Russel terrier was referred for syncopal episodes. An electrocardiogram revealed paroxysmal atrial flutter followed by periods of sinus arrest, suggesting sick sinus syndrome. Echocardiography showed severe biventricular wall thickening (hypertrophic cardiomyopathy (HCM) phenotype) with no signs of fixed or dynamic left ventricular outflow tract obstruction. Blood pressure, abdominal ultrasound, serum total thyroxin and thyroid-stimulating hormone, and insulin-like growth factor-1 were all within normal limits. Cardiac troponin I was elevated (1.7 ng/mL, ref<0.07). Serological tests for common infectious diseases were negative. A 24-h Holter confirmed that the syncopal episodes were associated with asystolic pauses (sinus arrest after runs of atrial flutter) ranging between 8.5 and 9.6 s. Right ventricular endomyocardial biopsies (EMB) were performed at the time of pacemaker implantation to assess for storage or infiltrative diseases that mimic HCM in people. Histological analysis of the EMB revealed plurifocal inflammatory infiltrates with macrophages and lymphocytes (CD3+ > 7/mm2) associated with myocyte necrosis, but no evidence of myocyte vacuolisation or infiltrative myocardial disorders. These findings were compatible with myocardial ischaemic injury or acute lymphocytic myocarditis. Molecular analysis of canine cardiotropic viruses were negative. The dog developed refractory congestive heart failure and was euthanised 16 months later. Cardiac post-mortem examination revealed cardiomyocyte hypertrophy and disarray with diffuse interstitial and patchy replacement fibrosis, and small vessel disease, confirming HCM. We described a systemic diagnostic approach to an HCM phenotype in a dog, where a diagnosis of HCM was reached by excluding HCM phenocopies.

Clinical presentation, management, and survival in dogs with persistent atrial standstill in the United Kingdom.

OBJECTIVES: To investigate the clinical and echocardiographic presentation of dogs with persistent atrial standstill (PAS), identify variables measured at first presentation that could predict their survival, and document the progression of the disease after pacing. MATERIALS AND METHODS: Retrospective study of medical records of dogs diagnosed with PAS at three referral hospitals of the United Kingdom over seven years. RESULTS: Twenty-six dogs were diagnosed with PAS during the study period. Median age of the population was three years (range: seven months-12.5 years). The most common clinical sign was syncope (14/26). Twenty-four dogs received artificial pacemakers (PM). Major complications after PM implantation were observed in four dogs (four/24). Serial echocardiographic examinations showed that cardiac dimensions of PAS dogs with left atrial or left ventricular dilation at first presentation did not return to reference range after pacing. Further dilation of the cardiac chambers, recurrence of congestive heart failure (CHF), or development of new episodes of CHF were documented in seven, four, and 10 PAS dogs, respectively, despite pacing. Median survival time for cardiac-related deaths after PM implantation was 1512 days (18-3207). Neither CHF nor echocardiographic variables at presentation predicted survival after PM implantation in PAS dogs. CONCLUSIONS: Persistent atrial standstill (PAS) is an uncommon bradyarrhythmia, occurring in young adult dogs. Affected dogs were often presented with syncope. Whilst syncope resolved, cardiac remodeling persisted after PM implantation. Long-term survival was favorable after PM implantation and was not predicted by congestive status or cardiac chamber size at first presentation.

The diagnostic utility of hypophosphatemia for differentiating generalized tonic-clonic seizures from syncope in dogs: A case control study.

Transient hypophosphatemia is often detected in humans following generalized tonic-clonic seizures (GTCS), and serum phosphorus concentration (sPi) serves as a marker to differentiate GTCS from syncope. The objective of this retrospective study was to assess the usefulness of hypophosphatemia as a diagnostic marker for GTCS in dogs. Eighty-seven and 26 client-owned dogs with GTCS or syncope, respectively, were enrolled. Dogs were included if the episode occurred ≤ 3 h from presentation, and if sPi and serum creatinine (sCr) were measured. Dogs were excluded if aged < 1 year or if sCr exceeded 176.8 µmol/L. There were no group differences in sCr. Hypophosphatemia (sPi ≤ 0.97 mmol/L) occurred in 28 dogs (32%) in the seizure group, and in no dogs in the syncope group. Median sPi was significantly (P < 0.001) lower in the seizure group (1 mmol/L, [range, 0.31-2.87 mmol/L]) compared to the syncope group (1.35 mmol/L [range, 0.97-2.71 mmol/L]). Furthermore, in dogs presented while seizing (n = 24/87; 28%) median sPi was significantly lower compared to those that were not (0.9 mmol/L [range, 0.3-1.74 mmol/L] vs. 1 mmol/L [range, 0.33-2.18 mmol/L], P = 0.050). ROC analysis of sPi as a marker of GTCS yielded an AUC of 0.757 (95% confidence interval 0.667-0.847), with an optimum cutoff point of 0.97 mmol/L, corresponding to specificity and sensitivity levels of 100% and 44%, respectively. In conclusion, sPi may, in certain cases, serve as an additional diagnostic tool to differentiate GTCS from syncope in dogs. Hypophosphatemia, especially with sPi < 0.97 mmol/L, may be useful in clinical practice to rule in GTCS.

Treatment of portal vein thrombosis using vascular access port implantation in a Dalmatian dog: A case report.

Background: Portal vein thrombosis is a disease with potentially deleterious outcomes including portal vein hypertension and intestinal infarction. The factors contributing is various; however, dogs with with acute portal vein thrombosis or multiple thromboses are less likely to survive. Therefore, acute development of portal hypertension has a requires an immediate treatment. Case Description: A 10-year-old Dalmatian was referred for syncope and azotemia, hyperammonemia. After each examinations including computed tomography scan, we diagnosed with acute portal vein thrombosis with unknown cause. A portal vein port was inserted to prevent and control the portal vein thrombus. The port was placed in abdomen subcutaneously after the position of the catheter were stabilized. Low-molecular-weight heparin was injected from the port to manage thrombosis after the operation. This case responded well to this treatment. Syncope and azotemia, hyperammonemia resolved and no relapse of thrombosis was found 6 months after the operation. Conclusion: Implantable vascular access port is a drug delivery system with the advantage of dealing with treatment-resistant acute portal vein thrombosis.

Quiet timer blanking in a dog with sick sinus syndrome and a permanent transvenous pacemaker.

A 14-year-old, 5.8 kg (12.7 lb) male castrated Jack Russell Terrier was referred for investigation of syncope and an arrhythmia. Electrocardiogram showed pronounced variation in the sinus rate including long periods of sinus arrest and an inconsistent escape rhythm. Sick sinus syndrome was the presumptive diagnosis. A single lead permanent transvenous pacemaker was implanted and was programmed to perform ventricular-demand pacing. Postoperative pacemaker interrogation revealed undersensing and asynchronous pacing during episodes of supraventricular tachycardia (SVT). This intermittent pacemaker malfunction was attributed to a specific pacemaker programming feature called quiet timer blanking. Adjustment of pacemaker parameters did not restore normal function. Treatment with sotalol (5 mg per os q 12 h) was used to medically treat the SVT, and asynchronous pacing was not observed during follow-up visits. To the authors' knowledge, this is the first documented case of quiet timer blanking causing paroxysmal undersensing and asynchronous pacing in a dog with a permanent pacemaker.

Successful application of closed loop stimulation pacemakers with remote monitoring in 3 miniature donkeys with syncope.

Rate-adaptive single chamber pacemakers with accelerometer, closed loop stimulation (CLS), and remote monitoring functionality (Eluna 8 SR-T, Biotronik, SE & Co, Germany) were implanted in 3 miniature donkeys with third-degree atrioventricular block and syncope. After recovery, different pacemaker programming modes were tested at rest, during stress without physical exercise and during physical exercise. Pacing rates were compared to actual atrial rates and showed that CLS functionality allowed physiological heart rate adaptation. A transmitter installed in the stable provided wireless connection of the pacemaker to the internet. Home monitoring was activated which performed daily wireless transmission of pacemaker functional measurements to an online server allowing diagnosis of pathological arrhythmias and pacemaker malfunction from a distance. Closed loop stimulation and remote monitoring functionality resulted in nearly physiological rate adaptation and allowed remote "from-the-stable" patient follow-up.

Characteristics and outcomes of cats with and without pacemaker placement for high-grade atrioventricular block.

INTRODUCTION: Available information on characteristics and outcome in cats with high-grade atrioventricular block (AVB) that receive a pacemaker is limited. ANIMALS: Twenty-two privately owned cats presenting with high-grade AVB. MATERIALS AND METHODS: Medical records were retrospectively examined. Cats were grouped as having received a pacemaker (PACE group) or not having received a pacemaker (non-PACE group). Clinical characteristics and outcomes of groups were evaluated. RESULTS: There were 10 cats in the PACE group and 12 cats in the non-PACE group. At presentation, syncope or seizure-like behavior (p = 0.004) and bradycardia (p = 0.043) were more common in the PACE than the non-PACE group. Historical lethargy (p = 0.015) and dull mentation (p = 0.045) were more common in the non-PACE group, as was clinically relevant systemic disease. Pacemaker placement improved syncope or seizure-like behavior in 100% of cats. The degree of AVB at presentation was not associated with pacemaker placement nor the future degree of AVB. The major complication rate of pacemaker placement was 40%. Intergroup survival was not significantly different (PACE group 1278 days, 95% confidence interval: 0-2145 days; non-PACE group 213 days, confidence interval: 1-not available, p = 0.77). CONCLUSIONS: Pacemaker placement improved clinical signs in cats with high-grade AVB. A difference in survival time could not be demonstrated between cats that received and did not receive a pacemaker in this retrospective study. High-grade AVB can be transient and accompanied by systemic disease in some cats.

Fluctuation of Clinical Signs With Near-Syncopal Episodes in a Dog With Gliomatosis Cerebri: A Diagnostic Challenge.

A 2-year-old Bull Mastiff cross Boxer neutered male dog was evaluated because of 2-month history of non-progressive right head tilt and mild vestibular ataxia. MRI of the brain revealed a faint T2W, FLAIR, DWI and ADC heterogenous hyperintense and T1W isointense intra-axial lesion with indistinct margins at the level of the pons and medulla oblongata. The lesion did not show any susceptibility artefact on T2* GRE images or contrast enhancement and CSF analysis was normal. Analysis of the spectra from MRS of the thalamus not promptly available at the time of the MRI study revealed a decreased level of NAA, as seen in people with gliomatosis cerebri. The dog represented 3 weeks later and, on this occasion, displayed left-sided head tilt, left-sided postural reaction deficits and near-syncopal episodes associated with state of confusion. Repeated MRI revealed a larger non-enhancing intra-axial lesion with a more hyperintense signal than previously described. CSF was normal and PCR of CSF for infectious diseases was negative. Thoracic and abdominal computed tomography did not reveal any primary or metastatic process. Immunosuppressive treatment was attempted and the dog remained stable over 5 days, then developed generalized tonic-clonic seizures which led to status epilepticus and death. Histopathology supported the diagnosis of gliomatosis cerebri. Gliomatosis cerebri remains difficult to diagnose ante-mortem, due to the broad age of onset and the variable duration and wide range of clinical signs. The mismatch between MRI findings and clinical presentation, the fluctuating clinical signs with near-syncopal episodes associated with a state of confusion, the presence of an infiltrative brain disease as depicted on MR imaging and a normal CSF analysis, should prompt the clinician to consider possible diagnosis of a widespread infiltrative neoplasm. Although, MRS may help narrow the differential diagnosis in favor of a neoplastic lesion, the overall prognosis remains poor.

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.

Identification and management of a subacute right ventricular perforation by an active-fixation permanent pacemaker lead in a dog.

A 5-year-old short-haired dachshund was referred with a history of repeated syncope associated with a third-degree atrioventricular block. A permanent transvenous pacemaker with an active-fixation lead was implanted. In the following 3 weeks, the syncopal episodes reappeared owing to a loss of ventricular capture. The pacemaker was reprogrammed to higher output, and effective pacing was re-established. Thoracic radiographs and echocardiography failed to identify any evidence of lead displacement. One month later, the patient presented a new episode of loss of capture. After fluoroscopy, cardiac perforation was suspected and subsequently confirmed by thoracotomy. An epicardial pacemaker lead was implanted without removing the perforating lead as there were no bleeding complications or damage to adjacent organs, and the length of time elapsed since implantation was assumed to have allowed for significant fibrotic adhesions to develop. Nineteen months after epicardial pacemaker implantation, endocardial lead dislodgement occurred. Simultaneously, the dog presented with gastrointestinal and respiratory abnormalities and severe thrombocytopenia. Once the dog was stabilized, the endocardial lead was percutaneously removed. One month later, loss of ventricular capture recurred. The owners declined any further treatment, and euthanasia was elected. Cardiac perforation after pacemaker implantation is an infrequent complication. In this case, the dog lived 22 months after subacute right ventricular perforation. Despite the poor prognosis associated with cardiac perforation by pacemaker leads, different approaches are possible to successfully manage this major complication. Extraction of the displaced lead remains controversial as, if the lead is not removed, late lead migration can occur.

Hemodynamics of tonic immobility in the American alligator (Alligator mississippiensis) identified through Doppler ultrasonography.

American alligators (Alligator mississippiensis) held inverted exhibit tonic immobility, combining unresponsiveness with flaccid paralysis. We hypothesize that inverting the alligator causes a gravitationally promoted increase in right aortic blood flowing through the foramen of Panizza, with a concurrent decrease in blood flow through the primary carotid, and thereby of cerebral perfusion. Inverting the alligator results in displacement of the liver, post-pulmonary septum, and the heart. EKG analysis revealed a significant decrease in heart rate following inversion; this decrease was maintained for approximately 45 s after inversion which is in general agreement with the total duration of tonic immobility in alligators (49 s). Doppler ultrasonography revealed that following inversion of the alligator, there was a reversal in direction of blood flow through the foramen of Panizza, and this blood flow had a significant increase in velocity (compared to the foraminal flow in the prone alligator). There was an associated significant decrease in the velocity of blood flow through the primary carotid artery once the alligator was held in the supine position. Tonic immobility in the alligator appears to be a form of vasovagal syncope which arises, in part, from the unique features of the crocodilian heart.

Canine case of swallowing syncope that improved after pacemaker implantation.

A 14-year-old intact male West Highland White Terrier weighing 6.9 kg was admitted to the Tokyo University of Agriculture and Technology Animal Medical Center with the complaint of syncope after showing signs of nausea during feeding. Sinus arrest induced by deglutition was confirmed using a Holter electrocardiography test. However, the clinical symptoms significantly improved after implantation of a permanent pacemaker. Seven months after implantation, the dog died from acute pancreatitis, a cause unrelated to the syncope. Immediately after its death, the heart, lungs, gastrointestinal tract, and other organs were dissected and examined histopathologically. The brain was also examined using magnetic resonance imaging. Examination results led to the diagnosis of swallowing-induced situational syncope.

Primary cardiac tumor presenting as left ventricular outflow tract obstruction and complex arrhythmia.

An adult female mixed breed dog presented for recurrent collapsing episodes over several weeks. Holter evaluation revealed periods of sinus arrest and echocardiography identified a soft tissue mass with subsequent severe dynamic obstruction of the left ventricular outflow tract. The patient was euthanized five days after presentation for severe dyspnea. Necropsy revealed an irregular mass circumferentially lining the left ventricular outflow tract as well as multiple myocardial metastases. The final diagnosis was an undifferentiated pleomorphic endocardial sarcoma.

Serum cardiac troponin I in canine syncope and seizures.

OBJECTIVE: To determine if serum cardiac troponin I (cTnI) concentration distinguishes between cardiogenic syncope and collapsing dogs presenting with either generalized epileptic seizures (both with and without cardiac disease) or vasovagal syncope. ANIMALS: Seventy-nine prospectively recruited dogs, grouped according to aetiology of collapse: generalized epileptic seizures (group E), cardiogenic syncope (group C), dogs with both epileptic seizures and cardiac disease (group B), vasovagal syncope (group V) or unclassified (group U). METHODS: Most patients had ECG (n = 78), echocardiography (n = 78) and BP measurement (n = 74) performed. Dogs with a history of intoxications, trauma, evidence of metabolic disorders or renal insufficiency (based on serum creatinine concentrations >150 µmol/L and urine specific gravity <1.030) were excluded. Serum cTnI concentrations were measured and compared between groups using non-parametric statistical methods. Multivariable regression analysis investigated factors associated with cTnI. Receiver operator characteristic curve analysis examined whether cTnI could identify cardiogenic syncope. RESULTS: Median cTnI concentrations were higher in group C than E (cTnI: 0.165 [0.02-27.41] vs. 0.03 [0.01-1.92] ng/mL; p<0.05). Regression analysis found that serum cTnI concentrations decreased with increasing time from collapse (p=0.015) and increased with increasing creatinine concentration (p=0.028). Serum cTnI diagnosed cardiogenic syncope with a sensitivity of 75% and specificity of 80%. CONCLUSIONS: Serum cTnI concentrations were significantly different between groups C and E. However, due to the overlap in cTnI concentrations between groups cTnI, measurement in an individual is not optimally discriminatory to differentiate cardiogenic syncope from collapse with generalized epileptic seizures (both with and without cardiac disease) or vasovagal syncope.

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.