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Syncope: Pathophysiology and Differential Diagnosis
Abstract
Syncope is a diagnostically challenging syndrome in humans and domestic animals. The pathophysiology of syncope is related to a short-term decrease in cerebral perfusion or cerebral delivery of oxygen or other essential nutrients. Syncope can be caused by cardiac disorders, reflex vagal syndromes, neurologic diseases, and metabolic abnormalities. A thorough history and physical examination as well as appropriate ancillary tests are needed to differentiate syncope from seizures, episodic weakness, and narcolepsy/cataplexy. Initial diagnostic steps include complete blood work, electrocardiography (ECG), and blood pressure measurements. Echocardiography with Doppler can be used to identify structural and functional cardiopulmonary abnormalities. Holter monitors, cardiac event recorders, and continuous in-hospital ECGs are useful in identifying arrhythmogenic causes. Although a definitive cause of syncope may not be identified, it is important to rule out cardiac causes because of their association with higher mortality.
... Diagnosis of the underlying cause of syncopal episodes may be challenging and requires an amulgamation of information on patient history, physical examination, biochemical profile, radiography, ECK and echocardiography. It was found that cardiovascular dysfunction, neurological disorders, and metabolic abnormality were the major causes of syncopal episodes (Davidow et al., 2001). In the present study, the dog presented with bradyarrythmia and the abnormal ECG findings could further confirmed the presence of cardiovascular dysfunction. ...
... Neurological problems resulting in syncopal episodes usually affect brain functions. Behavioral changes and alteration of neurological responses related to abnormal brain functions (Davidow et al., 2001) were not observed in the present case. Electrolyte imbalance leading to Table 1 Complete blood count before and after pacemaker implantation Table 2Pre-operative and post-operative blood chemistry profiles of the dog underwent pacemaker muscular weakness (Parent, 2007) was unlikely because major electrolytes were found within normal limit (Table 2). ...
A fourteen-year-old female neutered Schnauzer was presented to the hospital with multiple syncopal episodes for two weeks. The dog appeared fatigue and sleepy but remained responsive. Clinical examination revealed bradycardia and irregular pulse. Electrocardiography showed sinus rhythm with repetitively long episodes of sinus arrest over 3 seconds, indicating sick sinus syndrome. The dog eventually underwent a transvenous single chamber permanent pacemaker. She was followed up for a month after surgery without recurrent syncope and irregular heart rate.
Syncope is a sudden loss of consciousness associated with loss of postural tone (collapse) from which recovery is spontaneous. The evaluation of syncope in animals is often challenging. Regardless of the cause, the common denominator leading to all forms of syncope is decreased or brief cessation of cerebral blood flow. This chapter will describe the pathophysiology of syncope and focus on the cardiogenic causes and syncope‐like conditions.
Syncope may be caused by metabolic, vascular reflex, nervous or cardiac disturbances. Cardiac disturbances that may induce syncope include arrhythmias or disorders affecting ventricular filling and emptying. Diagnosis depends on a precise case history and rigorous clinical examination, plus ancillary tests (electrocardiogram, thoracic radiograph, serum-glucose concentration, etc.).
PART 1 of this three-part series (In Practice, January 2005, pp 16-28) described an aetiological and investigative approach to the collapsing dog, while Part 2 (In Practice, February 2005, pp 62-69) discussed the neuromuscular causes of collapse. This final article reviews the cardiovascular and miscellaneous causes of acute or episodic collapse.
Carotid body tumours were diagnosed in two British Bulldogs that each had a history of syncopal episodes induced by eating, drinking or pulling on the leash. In both dogs, a cervical mass was identified using computed tomography (CT) or magnetic resonance imaging, with carotid body tumour (CBT) being the histopathological diagnosis. A heart base mass was also identified in one dog by both CT and echocardiography. Swallowing syncope has been reported in the human literature in association with cervical mass lesions, but this is the first report in dogs. The present cases emphasise the value of advanced imaging of the head and neck in dogs presenting with clinical signs of syncope associated with swallowing and the importance of careful manipulation of the neck in patients with CBTs.
The most common presenting clinical signs of lung-lobe torsion include dyspnea, tachypnea, lethargy, and anorexia. Tussive syncope secondary to lung-lobe torsion has not been documented. This article describes the presentation, diagnosis, management, and outcome of a pug with tussive syncope secondary to lung-lobe torsion.
To retrospectively assess the long-term outcome for dogs that were presented with collapse, syncope or exercise intolerance for which an underlying cause is not identified.
The clinical records of animals presenting to two practices were assessed. Dogs which presented for collapse, syncope or exercise intolerance at least 6 months previously and did not receive a definitive diagnosis despite investigation were included. Follow-up of these cases was carried out by conducting telephone interviews with the owners.
One hundred and fifty-three cases were successfully followed up. Clinical signs had resolved in 64 cases (42%), 35 dogs (23%) were continuing to exhibit clinical signs, although 22 of these had improved without medical intervention. In 17 cases (11%), a diagnosis had subsequently been made or treatment was being administered and 37 dogs (24%) had died. Of the deaths, 18 (12%) were considered to be related to the original presentation. The overall prevalence of death and deterioration related to the problems investigated was 16·2% of cases. Death in boxers was significantly more common than in other breeds (36%).
Death and deterioration are uncommon outcomes for dogs other than boxers presenting with collapse, syncope and exercise intolerance for which a definitive diagnosis cannot be made.
Les syncopes récurrentes d'origine inexpliquée ou vasovagale affectent le fonctionnement physique et psychologique des patients vivant avec cette condition. Pourtant, peu de recherches se sont intéressées à comprendre la qualité de vie (QV) générale de ces patients, soit leur capacité à atteindre leurs objectifs dans différents domaines de vie, et les facteurs qui l'influence. Conséquemment, l'influence du sexe et du type de syncope sur la QV demeure inconnue. Qui plus est, aucune recherche n'a encore évalué les perceptions entretenues par les individus concernant leurs pertes de conscience. Pourtant, des études suggèrent que ces perceptions, appelées représentations de la maladie, affectent l'adaptation physique et psychologique des patients. L'incertitude entourant les causes et traitements des syncopes récurrentes suggère aussi l'importance d'explorer les perceptions des patients pour mieux comprendre leur influence sur la QV. Objectifs,Article 1 : Examiner les représentations de la maladie chez les hommes et les femmes souffrant de pertes de conscience récurrentes d'origine vasovagale (SVV) ou inexpliquée (SI) et référés pour un test de table basculante (TTB). Article 2 : Examiner la relation entre la QV, les représentations de la maladie, le sexe et le type de syncope chez les patients souffrant de syncope récurrentes référés pour un TTB. Méthode, Cent quinze (115) patients ont été interviewés un mois avant leur TTB à l'aide d'une entrevue semi-structurée et de questionnaires. Statistiques, Article 1 : les différences entre hommes et femmes et entre patients avec SVV et SI ont été examinées à l'aide d'une MANCOVA. Les représentations de la maladie ont également été catégorisées et explorées à l'aide de khi carrés et de comparaisons binomiales. Article 2, Une ANCOVA a permis d'évaluer l'association entre la QV, le sexe, le type de syncopes et les représentations de la maladie (les comparaisons entre les groupes de représentations de la maladie ont été faites selon les contrastes de type Helmert) en contrôlant pour l'âge et le nombre de syncopes. Une série de régressions linéaires ont permis d'explorer le rôle possible de médiateur des représentations de la maladie dans la relation entre le nombre de syncope et la QV. Résultats, Article 1 : les représentations sont similaires chez les hommes et les femmes ayant des SVV et des SI (tous les p > .10). Bien qu'entre 33% et 50% des patients ne savent pas quoi penser par rapport à leur maladie, l'exploration des réponses révèle divers patrons de représentations. Les patients ont des représentations émotionnelles et des représentations concernant la chronicité de leur condition très diversifiées. La majorité est indécise concernant le contrôle qu'ils peuvent exercer sur les syncopes et la durée cyclique (perception que les syncopes surviennent selon des cycles précis) de la condition. Peu de patients croient que les syncopes ont des conséquences sévères sur leur vie et qu'aucun traitement ne sera efficace pour les guérir. Seulement 19% des patients affirment ne pas être inquiet à propos de leur syncope. Finalement, très peu de patients (15%) ont le sentiment de comprendre leur condition. Article 2 : les résultats indiquent une QV réduite chez les patients avec syncopes récurrentes, particulièrement dans les domaines suivants: affectivité, cognitions, loisirs, travail et santé. Tous les patients ne rapportent toutefois pas une QV appauvrie. Les patients avec des représentations sévères ont une QV appauvrie (p = .022) comparativement aux individus ayant des perceptions peu ou moyennement sévères de leur syncope. Les hommes avec SI rapportent, quant à eux, la QV la plus faible comparativement aux hommes avec SVV, qui présentent une QV normale (p = .007). Finalement, les résultats suggèrent l'hypothèse d'un rôle médiateur des représentations de la maladie dans l'association entre le nombre de syncope et la QV. Conclusion,
les patients vivant avec des pertes de conscience récurrentes d'origine vasovagale ou inexpliquée affichent un manque de compréhension concernant leur condition et présentent des représentations variées à propos des syncopes. La QV est appauvrie, surtout chez les patients ayant des représentations plus sévères de leur condition et chez les hommes avec SI. Les résultats suggèrent donc un besoin d'éducation, ainsi que de support chez ces patients afin d'améliorer leur compréhension de leur problématique ainsi que leur QV. ______________________________________________________________________________ MOTS-CLÉS DE L’AUTEUR :Syncope récurrentes, Qualité de vie, Représentations de la maladie, Sexe et types de syncopes.
This case report describes transient atrioventricular block as the etiology for syncopal events in a 6-year-old male German shepherd dog with atrial fibrillation and dilated cardiomyopathy. The arrhythmia diagnosis was obtained via Holter monitoring. Medical treatment with a sustained-release preparation of theophylline, as an additive to the standard congestive heart failure treatment (benazepril, furosemide and pimobendan) may have contributed to temporary remission of the syncopal events. However, the congestive heart failure progressed and the dog was euthanized. Veterinarians should be aware of the possibility of transient atrioventricular block causing syncope in dogs with DCM and AF and should be careful in empirically lowering the ventricular response rate if these dogs present with syncopal episodes.
Tourette syndrome (TS) is familial neuropsychiatric disorder that is characterized by motor and phonic tics that begin in childhood. Once thought of as a rare and debilitating disorder, in the last decade new scientific knowledge suggests that TS and related tic disorders are more common and less debilitating for the majority of individuals. Evidence points toward a spectrum of TS symptomatology that extends beyond the tics disorder to probably include obsessive-compulsive disorder, attention deficit hyperactivity disorder, and mood disorders. Tourette syndrome and its differential diagnosis are discussed in this article with a focus on new developments in classification, etiology, epidemiology, genetics, pathophysiology, and clinical management.
Syncope is a common clinical presentation. Although most commonly benign, it may herald a pathology with a poor prognosis. The work-up of syncope includes a careful history, physical examination, electrocardiogram, risk stratification, and appropriately directed testing. The key factor in the investigation of syncope is the presence (or absence) of structural heart disease or an abnormal electrocardiogram. The most useful investigation in unexplained syncope with a normal heart is the tilt table test for evaluating predisposition to neurocardiogenic (vasovagal) syncope. In the setting of structural heart disease or an abnormal electrocardiogram, electrophysiologic studies play a more important role. The utility of noninvasive cardiac monitoring for symptom-rhythm correlation may be limited by infrequent symptoms. The availability of external and implantable loop recorders allows prolonged periods of monitoring to increase diagnostic yield. The management of patients with syncope may be complex. Early referral to a cardiac electrophysiologist is warranted in patients who are at high risk.
The objective of this study was to evaluate retrospectively the clinical utility of ambulatory (Holter) electrocardiographic monitoring in syncopal dogs and to compare the Holler recording with the clinic electrocardiogram (ECG) in these animals. Fifty Holter reports and 44 medical records from 44 dogs were evaluated. A syncopcal episode occurred during monitoring in 24% of the recordings. No obvious relationship was found between the frequency of syncope occurring before Holter recording and the likelihood of a dog having an episode during recording. Holter recordings were helpful in establishing a diagnosis 42% of the time, but no relationship was detected between the frequency of episodes occurring before Holler recording and the likelihood of a diagnostically useful Holter. An arrhythmia was ruled out as the cause of syncope in 12% of the recordings and was implicated as the cause of syncope in 30% of recordings. Of these, 20% were ventricular tachyarrhythmias and 10% were bradyarrhythmias including pacemaker failure. Ambulatory electrocardiographic recordings led to a therapeutic change in 38% of cases. A comparison of the Holter recordings and clinic ECGs documented the expected increased sensitivity for Holler detection of arrhythmias. The average clinic ECG heart rare consistently exceeded the average Holler heart rate with a mean difference between the average heart rates recorded by the two techniques of 31 bpm (range -8-87 bpm).
In acquired myasthenia gravis (MG), which is a relatively common immune-mediated disorder in dogs, autoantibodies are produced against nicotinic acetylcholine (ACh) receptors of skeletal muscle. These autoantibodies disrupt neuromuscular transmission; the disruption is manifested clinically as muscle weakness. Because it can present in various clinical forms, clinicians must maintain a high index of suspicion for acquired MG. Clinical forms include focal, generalized, and acute fulminating MG. Megaesophagus is commonly encountered in all forms of acquired canine MG; sometimes, megaesophagus is accompanied by evidence of aspiration pneumonia. Several tests are available for diagnosing acquired MG, including the edrophonium response test, an immunocytochemical test, measurement of serum ACh receptor antibody concentration via immunoprecipitation radioimmunoassay, and repetitive nerve-stimulation testing. A relatively new electrodiagnostic test in veterinary medicine, single-fiber electromyography, may be more widely used in the diagnosis of canine acquired MG in the future. A positive ACh receptor antibody concentration result confirms the diagnosis of acquired MG, but a negative result does not rule out the possibility of the disease. The first part of this two-part article discusses the pathophysiology, clinical features, and diagnosis of acquired MG in dogs. Part II will consider the treatment of the condition.
Available ambulatory electrocardiographic devices include 24-hour (Holter) monitors and event-based recorders (EBRs; event-based monitors). EBRs are smaller and less expensive, can be worn for longer periods, and are more versatile regarding transmission of the acquired electrocardiographic information than are Holter monitors. These characteristics have made EBRs useful in small animal practice. However, EBRs may miss asymptomatic arrhythmias and are not useful for monitoring antiarrhythmic drug therapy. Attachment and use of EBRs are technically simple, but owner participation is required to activate the recorder when the patient exhibits clinical signs. EBRs help to identify whether intermittent clinical signs are due to a cardiac arrhythmia; if they are, the monitor reveals the type of arrhythmia. This important information can then be of therapeutic value, as demonstrated in the clinical cases discussed in this article.
Cardiac tumors may represent mechanical causes for syncope by limiting left ventricular filling and/or by obstructing the left ventricular outflow tract. Malignant melanoma is known to metastasize to the myocardium or pericardium, but there are only a very limited number of reports describing endocardial involvement by the tumor. We describe herein an 84-year-old woman who presented with daily near-syncope episodes, 9 years after treatment for a choroidal melanoma. The echocardiography and the pathologic examination revealed a metastatic melanoma. This is the first reported case of an ocular melanoma metastasizing to the heart and presenting as a left ventricular intracavitary pedunculated mass.
An animal model, consisting of a particular line of purebred pug dogs is described. The dogs displayed spontaneous episodes of syncope characterized by sudden collapse, no detectable heart beat, cyanosis, and dilated pupils. The tendency for syncope and sudden death was transmitted through four generations. Measurements of blood electrolytes and routine necropsy and histopathologic examination did not provide explanations for the attacks or sudden deaths. Histologic examination of the cardiac conduction system did reveal abnormal narrowing of the midportion of the His bundle. Monitoring of the ECG for 4 to 6 hr by radiotelemetry demonstrated that 15 pugs had a higher frequency of nonconducted atrial beats due to second-degree AV heart block (8.02/hr) than did 11 normal mixed-breed dogs (0.36/hr). The AV block was related to the respiratory cycle and was prevented by atropine. Eight of the pugs and four mixed-breed dogs were monitored continuously by radiotelemetry for 2 to 6 weeks with the use of combinations selected from myocardial electrograms, surface ECG, arterial blood pressure, respiration, EEG, and surface laryngeal EMG. An automatic system was used to retain data associated with the absence of ventricular activation. Episodes of total cardiac standstill for 6 to 15 sec without the appearance of escape pacemakers were recorded from all the pug dogs. The episodes of cardiac standstill were of two distinct types. The first type appeared as a markedly exaggerated sinus arrhythmia. The second type was a sudden transition from a moderate tachycardia to cardiac standstill. Simultaneous time-lapse video monitoring of selected pugs revealed that the first type of cardiac standstill occurred when the dogs were resting or asleep. The second type occurred when they were awake; this second type of cardiac standstill was associated with the syncopal attacks which had been observed.
Syncope is a common but complex medical disorder with a multitude of etiologies, some of which are still not well understood. In a general population, the greatest diagnostic yield is from the history and physical examination. Numerous other diagnostic modalities include Holter monitoring, signal-averaged ECG, cardiac electrophysiology study, and tilt table testing. A defined etiology will not be determined for a large percentage of patients after such an extensive work-up. Management of patients is based on the cause of syncope and is difficult in those patients in whom an etiology cannot be established. The syndrome of neurally mediated syncope is a relatively recently appreciated entity and provides important clinical investigational challenges.
This article has no abstract; the first 100 words appear below.
HYPOTENSIVE states are well known to activate the sympathetic nervous system, leading to reflex vasoconstriction and tachycardia.¹ Hypovolemic hypotension, however, can be accompanied by paradoxical withdrawal of sympathetic drive, leading to vasodilation and bradycardia — responses that, in turn, exacerbate the decrease in blood pressure.²³⁴⁵ In humans, hypotension with an inappropriately normal or frankly decreased heart rate has been observed during hemorrhagic shock,⁶ after the infusion of vasodilators,⁷ and most recently, in response to the infusion of isoproterenol during the upright-tilt test, which is used to provoke syncope.⁸,⁹ The current belief is that this type of vasodepressor reaction is a . . .
Supported by grants to Dr. Scherrer from the Fondation Suisse de Bourses en Medecine et Biologie and from the Policlinique Médicale Universitaire, Lausanne, Switzerland; by grants to Dr. Vissing from the Danish Heart Foundation and the Danish Medical Research Council (12–6945 and 12–7663); by a National Research Service Award (HL08085) to Dr. Morgan from the National Heart, Lung, and Blood Institute; by grants to Dr. Victor from the Ruby D. Hexter Estate and the American Heart Association Texas Affiliate (86G-098 and 87R-085) and a Clinical Investigator Award (HL01886) and a Program Project Grant (HL06296) to Dr. Victor from the National Heart, Lung, and Blood Institute; and by a grant from the Lawson and Rogers Lacy Research Fund in Cardiovascular Diseases. Dr. Victor is an Established Investigator of the American Heart Association.
We are indebted to Jere H. Mitchell, M.D., for his continued encouragement and support, to Herbert A. Berkoff, M.D., for allowing us to study his patient, and to Janet Batjer for assistance in the preparation of the manuscript.
Source Information
From the Cardiology Division, Department of Internal Medicine, and the Harry S. Moss Heart Center, University of Texas Southwestern Medical Center at Dallas (U.S., S.V., B.J.M., R.G.V.), and the Cardiology Section, Department of Medicine, University of Wisconsin, Madison (P.H.). Address reprint requests to Dr. Victor at the Cardiology Division, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75235–9034.
Clinical signs of bradycardia and syncope, associated with intracranial meningioma, were observed in a 4-year-old female Irish Setter. Electrocardiographic abnormalities confirming bradycardia and suggestive of sinoatrial arrest were demonstrated. Return to a normal heart rate and sinus rhythm after administration of atropine IV indicated that increased vagal tone was responsible for the observed abnormalities. Neither glycopyrrolate nor propantheline bromide therapy was successful in controlling bradycardia and syncope. Necropsy findings included the demonstration of a 3 X 2 X 2-cm mass on the ventral aspect of the right half of the brain. This mass covered half of the mammillary body and extended as a thick reddish brown membrane extending over the piriform lobe of the cerebrum, optic chiasm, and longitudinal fissure. Histologically, the mass was identified as a meningotheliomatous meningioma.
Ventricular preexcitation was diagnosed in 6 dogs and 7 cats examined because of weakness, syncope, or congestive heart failure, and as an incidental finding in 1 dog and 2 cats. Reciprocating tachycardias were documented in 8 of the cases. Six of the cats had a pathologic diagnosis of primary cardiomyopathy. Two of the dogs had an associated congenital heart defect. Reciprocating tachycardias were controlled in 4 cases with digoxin, in 2 cases with propranolol, and in 1 case with quinidine. Conduction through the accessory pathway was altered by quinidine (2 cases), digoxin, and propranolol (1 case each), resulting in a lengthened P-R interval and more normal QRS complex configuration.
Impulse activity in vagal afferent fibres and changes in heart rate were simultaneously recorded during rapid hemorrhage or blood pooling in cats in order to elucidate whether the sudden reflex bradycardia, sometimes evoked with the mentioned interventions, was correlated to an increased activity in any type of heart receptors. The results show that the slowing of the heart, resulting from an emptying of the central blood reservoirs was correlated to, and preceded by, an increased activity in receptors located in the left ventricle and signalling in non-medullated afferents. The receptors were found to be activated also by obstructions of the ascending aorta and mechanical stimulation of the heart, and therefore seem to operate as mechanorecepton, stimulated by a “distortion” of the myocardium. - It is conceivable that with rapid bleeding or pooling of blood, the receptors are excited by an improper squeezing of the myocardium when the ventricles contract vigorously around an almost empty chamber, and then induce a reflex bradycardia. This reflex mechanism, resembling the so-called vaso-vagal syncope reaction in man, may therefore serve as a protective system causing a break on the heart and allowing for an improved diastolic filling in situations when venous return is critically reduced.
One hundred seventy patients with syncope presenting to an emergency department were studied prospectively. A checklist was used to supplement the physician's history and physical to ensure adequate recording of potentially useful data. Follow-up data were available in 89% of patients with a mean follow-up period of 6.2 months. Patients were categorized by presumed etiology using specific criteria. Typical vasovagal syncope occurred in 37.1% of patients. Other etiologies included first seizure (8.8%), orthostasis (7.6%), cardiac (4.1%), micturition (2.4%), hypoglycemia (1.8%), and psychogenic (0.6%). Syncope of unknown etiology accounted for 37.6% of the patients. The estimated duration of warning period was significantly shorter in patients with cardiac syncope compared to patients with vasovagal syncope. The yield of laboratory tests was low with the exception of the serum bicarbonate, which was decreased in 70% of our seizure patients. Recommendations regarding initial evaluation and admission are discussed.
We prospectively evaluated and followed 204 patients with syncope to determine how often a cause of syncope could be established and to define the prognosis of such patients. A cardiovascular cause was established in 53 patients and a noncardiovascular cause in 54. The cause remained unknown in 97 patients. At 12 months, the overall mortality was 14 +/- 2.5 per cent. The mortality rate (30 +/- 6.7 per cent) in patients with a cardiovascular cause of syncope was significantly higher than the rate (12 +/- 4.4 per cent) in patients with a noncardiovascular cause (P = 0.02) and the rate (6.4 +/- 2.8 per cent) in patients with syncope of unknown origin (P less than 0.0001). The incidence of sudden death was 24 +/- 6.6 per cent in patients with a cardiovascular cause, as compared with 4 +/- 2.7 per cent in patients with a noncardiovascular cause (P = 0.005) and 3 +/- 1.8 per cent in patients with syncope of unknown origin (P = 0.0002). Patients with syncope can be separated into diagnostic categories that have prognostic importance. Patients with a cardiovascular cause have a strikingly higher incidence of sudden death than patients with a noncardiovascular or unknown cause.
Neurocardiogenic syncope is a common medical problem that can be identified easily by history and the findings of the head-up tilt test. Depressor reflexes from the heart causing sympathetic withdrawal that, in turn, lead to peripheral vasodilatation and hypotension may have an important role in the pathogenesis of neurocardiogenic dysfunction. Once a diagnosis of neurocardiogenic syncope has been made, specific therapeutic strategies can usually prevent recurrent syncope. However, the natural history of neurocardiogenic syncope has not been studied. Double-blind placebo-controlled studies or drug withdrawal trials are needed to assess whether all patients with neurocardiogenic syncope need lifelong therapy.
Rapid, clinical supraventricular tachycardia (SVT), without apparent underlying heart disease, was identified in 3 young Labrador Retrievers and 1 Labrador Retriever-type dog. The electrocardiographic characteristics, identification of ventricular preexcitation in 2 dogs, age at onset, response to antiarrhythmic agents, and recent electrophysiologic documentation of a concealed accessory pathway in another young Labrador Retriever suggested orthodromic atrioventricular reciprocating tachycardia as the mechanism of SVT.
This study was done to evaluate pacemaker therapy for severe recurrent vasovagal syncope.
Nonrandomized studies have suggested that permanent pacing might help control the symptoms of recurrent vasovagal syncope. The study goal was to evaluate the effect of permanent pacemaker implantation on syncope in patients with frequently recurrent vasovagal syncope.
Patients with > or = 6 lifetime episodes of syncope and with a tilt-table test that induced syncope or presyncope, as well as a relative bradycardia, were randomized to receive a dual-chamber pacemaker or not. The pacemaker prevented bradycardia and provided high-rate pacing if a predetermined drop in heart rate occurred (rate-drop response). The primary outcome was the first recurrence of syncope. Patients also completed a detailed diary recording presyncopal episodes.
A total of 284 patients was originally planned and a pilot study of 60 patients was initiated. At the planned first formal interim analysis of efficacy of the pilot study, an unanticipated large treatment effect was observed which fulfilled the prespecified criteria for early termination of the study. At that time, there were 54 patients enrolled, randomized evenly to no pacemaker or to pacemaker. In the no-pacemaker and pacemaker groups the mean ages were 40 and 46 years; 74% and 70% patients, respectively, were female. The baseline tilt-table test showed a slowest heart <60/min or longest heart period >1000 ms in 60% of no-pacemaker patients and 72% of pacemaker patients. There was a marked reduction in the postrandomization risk of syncope in pacemaker patients (relative risk reduction 85.4%, 95% confidence interval 59.7% to 94.7%; 2p=0.000022).
Dual-chamber pacing with rate-drop response reduces the likelihood of syncope in patients with recurrent vasovagal syncope.
The cause of syncope often eludes the clinician despite extensive efforts to make a definitive diagnosis. In that group of patients for whom the cause has eluded the clinician, it is unclear which patients need a rapid inpatient work-up and which patients can be safely discharged for outpatient evaluation. The authors present the results of a systematic literature search to determine the diagnostic value of the emergency department work-up of the patient with syncope.
We report a patient who experienced cough-induced syncope secondary to transient complete heart block.
Pulmonary hypertension occurs as a primary or secondary disorder of the pulmonary vasculature. Doppler echocardiography provides a noninvasive tool for the estimation of pulmonary arterial pressure when tricuspid regurgitation or pulmonic insufficiency is present. The cardiology database at Colorado State University was reviewed, and echocardiographic records from cases diagnosed with pulmonary hypertension were evaluated. Application of the modified Bernoulli equation to the maximal instantaneous velocity of a right-sided regurgitant jet provided evidence of pulmonary hypertension in 53 dogs over a 4-year period. Tricuspid regurgitant velocity > or = 2.8 m/second or pulmonic insufficiency velocity > or = 2.2 m/second was considered abnormal and indicative of pulmonary hypertension. Tricuspid regurgitant gradients in 51 dogs ranged from 32 to 145 mm Hg (mean, 63.0 mm Hg; median, 57.0 mm Hg; 25th-75th percentiles, 45.2-76.5 mm Hg). Pulmonic insufficiency gradients in 8 dogs ranged from 20 to 100 mm Hg (mean, 59.5 mm Hg; median, 61.5 mm Hg; 25th-75th percentiles, 32.0-84.5 mm Hg). Affected dogs ranged in age from 2 months to 16 years. Clinical signs were characteristic of cardiopulmonary disease, but a relatively high frequency of syncope was noted (12 of 53 dogs, 23%). Pulmonary hypertension was probably due to increased pulmonary vascular resistance in 23 dogs, pulmonary overcirculation in 2 dogs, and pulmonary venous hypertension in 23 dogs. Five dogs lacked a clinically recognizable cardiopulmonary cause of pulmonary vascular disease. Our results suggest that pulmonary hypertension can occur as a complication of commonly encountered cardiopulmonary diseases, and that Doppler echocardiography can facilitate recognition of this condition.
To determine the clinical usefulness of cardiac event recording in evaluating dogs and cats with unexplained syncope, episodic collapse, or intermittent weakness.
Retrospective study.
58 dogs and 2 cats.
Medical records and electrocardiographic rhythm strips obtained by cardiac event recordings were reviewed. Cardiac rhythm data from the event recordings were classified as diagnostic or nondiagnostic. Diagnostic yield was calculated by dividing the number of animals for which cardiac event recording was diagnostic by the total number of animals undergoing cardiac event recording.
For 51 animals, cardiac event recording was classified as diagnostic; therefore, overall diagnostic yield was 85%. Diagnostic yield was lower for animals without underlying structural heart disease (75.5%) than for animals with structural heart disease (95.6%). A specific arrhythmia was identified as the cause of clinical signs in 18 of the 51 (35%) animals for which cardiac event recording was diagnostic. Cardiac arrhythmia was definitively excluded as the cause of clinical signs in the remaining 33 (65%) animals in which cardiac event recording was diagnostic.
Results indicate that cardiac event recording had a high diagnostic yield in dogs and cats examined because of unexplained syncope, episodic collapse, or transient weakness and ataxia, regardless of whether animals did or did not have an underlying structural heart disease. Diagnostic yield of cardiac event recording was higher than that reported previously for Holter monitoring.
Cardiac tumors may represent mechanical causes for syncope by limiting left ventricular filling and/or by obstructing the left ventricular outflow tract. Malignant melanoma is known to metastasize to the myocardium or pericardium, but there are only a very limited number of reports describing endocardial involvement by the tumor. We describe herein an 84-year-old woman who presented with daily near-syncope episodes, 9 years after treatment for a choroidal melanoma. The echocardiography and the pathologic examination revealed a metastatic melanoma. This is the first reported case of an ocular melanoma metastasizing to the heart and presenting as a left ventricular intracavitary pedunculated mass.
A case of hypertrophic cardiomyopathy in a dromedary camel (Camelus dromedarius) is described for the first time. The patient, a castrated 9-year-old animal, presented with a 6-month history of several episodes of syncope after moderate exercise and later at rest. The syncope had a sudden onset and a duration of 30 to 45 seconds. After clinical, electrocardiographical and echocardiographical examination, a tentative diagnosis of hypertrophic cardiomyopathy was made. At necropsy, the heart had a globose shape and was firm on palpation. The left ventricular free wall and the interventricular septum were thickened in cross-section and the left ventricular lumen was small. The clinical diagnosis was confirmed by histologic examination of heart tissue that demonstrated hypertrophy of myocardial fibres with vesicular nuclei and the presence of diffuse interstitial fibrosis.