Canine microsatellites associated with genes implicated in cardiac development and function.
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Animals↗
Biomedical subjects
N S Moïse
Publications and source records attributed to N S Moïse.
Long-term monitoring of animal models of sudden death.
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Animals↗
Temporal organization of atrial activity and irregular ventricular rhythm during spontaneous atrial fibrillation: an in vivo study in the horse.
INTRODUCTION: Atrial fibrillation (AF) is common in healthy horses. We studied the temporal organization of AF to test the hypothesis that the arrhythmia is governed by a high degree of periodicity and therefore is not random in the horse. Further, we surmised that concealed conduction of AF impulses in the AV node results in an inverse relationship between AF frequency and ventricular frequency. METHODS AND RESULTS: Fast Fourier transform (FFT) analysis of atrial activity was done on signal-averaged ECGs (n = 11) and atrial electrograms (n = 3) of horses with AF at control (C), after quinidine sulfate (22 mg/kg by mouth every 2 hours) at 50% time to conversion (T50), and immediately before conversion (T90) to sinus rhythm. FFT always revealed a single dominant frequency peak. The mean dominant frequency decreased until conversion (C = 6.84 +/- 0.85 Hz, T50 = 4.87 +/- 1.5 Hz, T90 = 3.41 +/- 1.18 Hz; P < 0.001). Mean AA intervals (n = 500) gradually increased after quinidine. Mean RR intervals (n = 500), standard deviation of the mean (SDM), Poincaré plots, and serial autocorrelograms (SACs) of 500 RR intervals were measured at C and T90 to determine the ventricular response to AF and quinidine-induced changes in the variability of the ventricular response. Mean RR interval and SDM were reduced after quinidine (C = 1431 +/- 266 msec and 695 +/- 23 msec; T90 = 974 +/- 116 msec and 273 +/- 158 msec, respectively; P < 0.01). Poincaré plots and SAC at C and at T90 revealed a significant correlation of consecutive RR intervals typical of a system with a deterministic behavior. At T90, the variability of RR intervals was reduced and the overall periodicity of RR intervals was increased after quinidine administration. CONCLUSION: In the horse, AF is a complex arrhythmia characterized by a high degree of underlying periodicity. The inverse AA-to-RR interval relationship and reduced variability of RR intervals after quinidine suggest that the ventricular response during AF results from rate-dependent concealment of AF wavelets bombarding the AV node, which nevertheless results in a significant degree of short-term predictability of beat-to-beat changes in RR intervals.
Animals↗
Introduction of an endocardial pacing lead through the costocervical vein in six dogs.
Lead dislodgement is one of the most common complications of endocardial pacing lead implantation in dogs. Incidence of lead displacement appears to be higher in large-breed, compared with small-breed, dogs, suggesting that excessive neck movements may be a contributing factor. To avoid introducing pacing leads through a vein in the neck, we developed a technique for implantation of endocardial pacing leads through the right costocervical vein. A right second intercostal space thoracotomy was performed to expose the vein, and the pacing generator was placed in the musculature over the lateral aspect of the thorax. The technique was performed in 6 dogs, 5 of which had had an endocardial pacing lead dislodge. None of the dogs had problems with lead dislodgement during follow-up periods of 15 to 20 months. Implantation of endocardial pacing leads through the costocervical vein should not be considered a replacement for implantation through the jugular vein. However, we believe that this technique is indicated for large dogs in which endocardial pacing leads implanted through the jugular vein have dislodged.
Animals↗
Inherited arrhythmias in the dog: potential experimental models of cardiac disease.
Centuries of inbreeding the domestic dog has resulted in numerous spontaneous breed-specific and familial diseases of all body systems [1]. Although few animal models of spontaneous arrhythmic death exists [2] veterinary cardiologists have recognized potentially inherited arrhythmias in the dog for years. The purpose of this paper is to describe the proven inherited, and the likely inherited, arrhythmias diagnosed commonly in the dog with the intent to provide information of potential models for investigation of primary arrhythmias. Additionally, examples of common arrhythmias that are secondary to inherited cardiac disease in the dog will be provided.
Animals↗
From cell to cageside: autonomic influences on cardiac rhythms in the dog.
The autonomic nervous system is pivotal in the characteristics of normal and abnormal cardiac rhythms. Some of the unique features (pronounced sinus arrhythmia and wandering pacemaker) of the canine electrocardiogram can be explained by the influence of parasympathetic tone. Perturbations that enhance the sympathetic nervous system can also potentiate arrhythmias, or counteract antiarrhythmic action. Moreover, disorders of the innervation to the heart may actually cause some life-threatening arrhythmias. This article reviews the interactions of the autonomic nervous system and cardiac rhythms as they pertain to the normal dog, as well as to specific arrhythmias in the boxer and German shepherd dog. Emphasis is placed on relating information from electrophysiological investigations to the clinical arena, thus demonstrating the value of linking the basic and clinical sciences as one medicine: knowledge from cell to cageside.
Animals↗
Diagnosis of inherited ventricular tachycardia in German shepherd dogs.
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Age Factors↗
Age dependence of the development of ventricular arrhythmias in a canine model of sudden cardiac death.
OBJECTIVES: The age-dependence of the development of ventricular arrhythmias was studied in German shepherd dogs with inherited ventricular arrhythmias and sudden death. BACKGROUND: A colony of German shepherd dogs has been established that exhibit inherited ventricular arrhythmias and sudden death. The incidence of arrhythmias increases with age. Because ventricular tachycardia is associated with bradycardia, it was hypothesized that the increased incidence of arrhythmias was related to age-dependent slowing of heart rate. METHODS: Arrhythmia counts and RR intervals were measured from serial ambulatory ECG recordings obtained in 71 dogs (1-48 weeks). In addition, 19 dogs were challenged with phenylephrine (10 micrograms/kg i.v.) at 15, 28, and 45 weeks of age, 10 dogs were challenged with epinephrine (1 microgram/kg i.v.) at 3, 5, 7, 9, 11, 18, and 28 weeks of age, and 10 dogs were challenged at 28 weeks with epinephrine (2.5 micrograms/kg i.v.), before and after propranolol (0.5 mg/kg i.v.). RESULTS: The incidence and severity of ventricular arrhythmias increased between 7 and 28 weeks of age and decreased between 28 and 44 weeks of age. The age-dependent increase in the incidence of ventricular tachycardia was associated with age-dependent reductions in sinus rate. Baroreflex-mediated slowing of the heart rate unmasked arrhythmias in young animals that did not spontaneously display arrthythmias and exacerbated existing arrhythmias in older animals. However, the magnitude of baroreflex-induced bradycardia was similar from 7-18 weeks of age, yet the incidence of arrhythmias increased progressively. Moreover, the waning of ventricular arrhythmias in older animals was not associated with more rapid sinus rates. CONCLUSION: The risk for sudden death in dogs with inherited ventricular arrhythmias increases with age in part because of age-dependent slowing of heart rate and in part because of other heart-rate-independent factors. The correspondence between the development of ventricular tachycardia and sinus pauses is consistent with the hypothesis that ventricular arrhythmias are initiated by early afterdepolarization-induced triggered activity.
Aging↗
An animal model of spontaneous arrhythmic death.
Ventricular arrhythmias and the proclivity for sudden death have been identified in German shepherd dogs. This disorder is inherited, and affected animals can be consistently produced from an established colony. The arrhythmias are most prevalent in young dogs between 22 and 26 weeks of age, with death most frequent at this same age. Death occurs most frequently during presumed sleep or at rest after exercise or excitement. The QT interval is not prolonged; however, more frequent notching of the T wave exists in affected dogs compared to control dogs. Polymorphic rapid nonsustained ventricular tachycardia occurs most frequently following long RR intervals. Accordingly, perturbations that decrease the heart rate or enhance sinus arrhythmia increase the incidence of ventricular arrhythmias. Because the arrhythmias are age, behavior, and heart rate dependent, the autonomic nervous system may play a role in their generation. As determined by metaiodobenzyl-guanidine scintigraphy and immunocytochemical staining of tyrosine hydroxylase, cardiac sympathetic innervation is regionally deficient in affected dogs. Evidence suggests that initiation of the ventricular arrhythmias is caused by early afterdepolarization (EAD)-induced triggered activity originating from left ventricular Purkinje fibers. Alpha 1-adrenergic stimulation provokes EADs in the Purkinje fibers and ventricular arrhythmias in the dogs. The development of EADs may be related to heterogeneity of repolarizing currents (Ito in particular) in affected dogs. From this canine model of spontaneous ventricular arrhythmias, the opportunity exists to investigate the interplay between abnormal development of cardiac innervation and the genesis of lethal ventricular arrhythmias.
Animals↗
Triggered activity as a mechanism for inherited ventricular arrhythmias in German shepherd Dogs.
OBJECTIVES: This study sought to determine whether early afterdepolarization-induced triggered activity is responsible for the initiation of ventricular arrhythmias in dogs with an inherited predisposition to sudden death. BACKGROUND: We have identified a colony of German shepherd dogs that display inherited ventricular ectopic activity and sudden cardiac death. The arrhythmias in these animals are pause dependent but are not associated with a prolonged QT interval, suggesting that they might be initiated by early afterdepolarization-induced triggered activity in Purkinje fibers. METHODS: Cardiac Purkinje fibers obtained from dogs that either did or did not exhibit ventricular tachyarrhythmias at the time of study were superfused in vitro with normal Tyrode solution (extracellular potassium ion concentration 4 mmol/liter) and were studied using standard microelectrode techniques. RESULTS: Early afterdepolarizations and triggered activity occurred spontaneously in Purkinje fibers obtained from affected dogs (n = 7) but not in fibers obtained from unaffected dogs (n = 13). Exit conduction block of triggered responses occurred to varying degrees within the Purkinje fiber but not at the Purkinje-muscle junction. Overdrive pacing suppressed triggered activity. The reemergence of triggered activity after cessation of pacing was both time and rate dependent. Triggered activity in fibers obtained from affected dogs was potentiated by phenylephrine and epinephrine and was suppressed by isoproterenol. Triggered activity was not induced by phenylephrine or epinephrine in fibers obtained from unaffected dogs. CONCLUSIONS: These results support the hypothesis that early afterdepolarization-induced triggered activity in Purkinje fibers is responsible for the initiation of ventricular arrhythmias in this canine model of inherited sudden death.
Adrenergic alpha-Agonists↗
Phenylephrine-induced ventricular arrhythmias in dogs with inherited sudden death.
INTRODUCTION: Dogs with an inherited predisposition to sudden death display ventricular arrhythmias having certain characteristics, such as pause dependence, that are suggestive of early afterdepolarization-induced triggered activity. We hypothesized that alpha-adrenergic stimulation may facilitate the development of these arrhythmias by inducing a reflex bradycardia and by exerting a direct myocardial effect. METHODS AND RESULTS: Twenty affected dogs and 7 unaffected dogs were studied. The incidence and severity of ventricular arrhythmias were determined after administration of phenylephrine (0.01 mg/kg IV), with or without pretreatment with propranolol (0.1 to 0.3 mg/kg IV), atropine (0.04 mg/kg IV), or prazosin (0.5 mg/kg IV). Third-degree heart block was induced by AV nodal ablation in 4 affected dogs. Phenylephrine increased ventricular arrhythmias in affected dogs, with or without pretreatment with propranolol, but did not induce ventricular arrhythmias in unaffected dogs. In dogs with intact AV nodal conduction, atropine increased sinus rate, which suppressed baseline and phenylephrine-induced arrhythmias. In dogs with heart block, arrhythmias were increased during baseline and after phenylephrine, with or without pretreatment with atropine. Prazosin and overdrive ventricular pacing suppressed phenylephrine-induced arrhythmias. CONCLUSION: Phenylephrine increases ventricular arrhythmias in dogs with inherited sudden death via both an induction of reflex bradycardia and a direct myocardial effect. Superimposition of heightened alpha-adrenergic and vagal tone may facilitate the development of sudden death in these animals.
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Relationship of ventricular tachycardia to sleep/wakefulness in a model of sudden cardiac death.
Death from some childhood disorders such as sudden infant death syndrome and the congenital long QT syndrome are associated with specific behaviors such as sleep or emotional stress. We studied young German shepherd dogs that die suddenly during presumed sleep. These dogs have inherited ventricular tachycardia (VT) which is most frequent during sinus bradycardia and sinus arrhythmia. We hypothesized that the number of VT complexes (three or more consecutive ectopic complexes) would be greatest during sleep. Moreover, we hypothesized that pauses in the sinus rhythm of greater than 1000 ms would be greatest in the behavior with the most frequent VT. Behavioral states [excited, ambulatory, sitting, lying, rapid eye movement (REM) sleep] were quantified from 24-h video recordings of seven dogs. VT and pauses were quantified for each behavior using simultaneously recorded ECGs. A multivariate model was used to analyze the results. After controlling for time of day, lying, and REM sleep were significantly (p < 0.02) associated with VT, whereas more active behaviors were not. Time of day also independently affected the number of VT complexes. However, behavior and time of day did not account for all of the variability in the number of VT complexes. Pauses were significantly associated with behavior, with the highest number of pauses occurring during lying and REM sleep. However, pauses were not always associated with VT, indicating that a pause was a necessary, but not sufficient, condition for the development of VT. These results suggest that modulation of VT incidence in these animals is multifactorial and that the highest number of VT complexes is associated with the bradycardia that accompanies REM sleep.
Animals↗
Right atrioventricular valve malformation in dogs and cats: an electrocardiographic survey with emphasis on splintered QRS complexes.
The purposes of this study were 2-fold: (1) to determine the prevalence of splintered QRS complexes (Rr', RR', rR', rr') and other electrocardiographic abnormalities in dogs and cats with congenital right atrioventricular valve malformation (RAVM) and (2) to determine if the Labrador Retriever was at greater risk for RAVM and splintered QRS complexes. EKGs from 39 dogs and 6 cats with echocardiographically diagnosed RAVM were studied retrospectively. Splintered QRS complexes were commonly found in affected Labrador Retrievers (9 of 19, 47%), non-Labrador Retrievers (12 of 20, 60%), and cats (4 of 6, 67%). Right ventricular enlargement was most commonly detected by precordial leads (CV6LL[V2], CV6LU[V4]) in the dogs and by the standard limb leads in the cats. Arrhythmias were uncommon. The Labrador Retriever was significantly overrepresented (P < .001) In the RAVM group when compared to the general hospital population (50% versus 8%). Males were also significantly overrepresented (P < .01). It was concluded that splintered QRS complexes are a distinctive and common electrocardiographic finding in dogs and cats with RAVM. Moreover, this congenital cardiac defect is most common in the Labrador Retriever, although this breed does not have proportionately more or less splintering of the QRS complexes than other breeds.
Animals↗