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Bradycardia-tachycardia syndrome due to sinus node disease and concealed Wolff-Parkinson-White syndrome.

A 75-year-old woman was admitted to the hospital because of a supraventricular tachycardia, long sinus pauses and ventricular tachycardia of the torsades de pointe type. Temporary ventricular pacing suppressed ventricular arrhythmias but supraventricular tachycardia persisted. An electrophysiologic study revealed the coexistence of sick sinus syndrome and circus movement tachycardia due to a concealed left-sided accessory atrioventricular pathway. This case represents a previously undescribed form of the bradycardia-tachycardia syndrome.

Aged↗

Electrophysiology and indications for pacing in the '80's.

Newer electrophysiological studies have improved our understanding of the pathogenesis of cardiac arrhythmias. Bradycardias originate either from a dysfunction of impulse formation in the sinoatrial node or from a disturbed conduction of the impulse. Different pathogenetic mechanisms are discussed as causes of tachyarrhythmias: circus movement (re-entry) is primarily due to pathological changes in conduction and refractoriness. Focal impulse formation results from local disturbances of depolarization and repolarization of the cell membrane: increased automaticity, abnormal automaticity, triggered activity. Symptomatic bradycardias still represent the standard indication for cardiac pacing particularly with implantable pacemakers. Based on clinical electrophysiology, various types of pacemakers are available at present: atrial triggered and atrial pacing pacemakers, AV-sequential pacemakers, ventricular demand-pacemakers, stand-by pacemakers, and fixed rate pacemakers. The multiprogrammability of newer pacemaker devices is a very useful tool in avoiding secondary interventions. For antitachycardia pacemaker therapy there are essentially three methods in use: 1. overdrive pacing to prevent re-entry phenomena and automaticity and also to suppress tachyarrhythmias based on increased or abnormal automaticity; 2. competitive stimulation for termination of tachycardias by means of single impulses; and 3. rapid atrial stimulation to convert atrial flutter into atrial fibrillation and consequently to normal sinus rhythm. In very rare cases rapid ventricular stimulation is mandatory. The positive results achieved with temporary stimulation methods have led to the development of permanent (implantable) antitachycardia pacemakers for long-term therapy, which have proven to be a low-risk alternative in drug-resistant tachyarrhythmias.

Anti-Arrhythmia Agents↗

Clinical experience with a new software-based antitachycardia pacemaker for recurrent supraventricular and ventricular tachycardias.

The Intermedics Intertach 262-12 tachycardia reversion pulse generator was implanted in 14 patients (six male, eight female, mean age at implantation 45 +/- 16 years) with recurrent symptomatic tachycardias. Six patients had atrioventricular (AV) nodal reentrant tachycardia, three patients had orthodromic tachycardia with Wolff-Parkinson-White syndrome, two had circus movement tachycardia via a concealed bypass tract, two had ventricular tachycardia, one patient had atrial flutter. Mean duration of symptoms before implantation was 8 +/- 4 years and mean number of antiarrhythmic drug trials was 3.5 +/- 1. The primary tachycardia response made consisted of autodecremental pacing in one patient, burst pacing in two patients, and adaptive scanning of the initial delay or burst cycle length in eleven patients. The secondary tachycardia response mode consisted of autodecremental pacing in four patients, burst pacing in three patients and burst scanning in four patients. Tachycardia response was automatic in all but one patient with ventricular tachycardia. During a follow-up period of 30.5 +/- 10.6 months, one patient with ventricular tachycardia died from a nonarrhythmic cause. Reinterventions were necessary due to electrode fracture in one patient and due to pacemaker software defect in another one. Two patients underwent surgical cure of their arrhythmia: one patient with atrial flutter and one patient with AV nodal reentry tachycardia, 24 months and 11 months postpacemaker implantation, respectively. Four patients required digitalis to prevent pacing induced atrial fibrillation. Other proarrhythmic effects were not encountered. The pacemaker proved to be a versatile system with reliable tachycardia detection and termination functions. It provided a valuable adjunctive therapy in these selected patients.

Adult↗

Effects of isoflurane on electrophysiological measurements in children with the Wolff-Parkinson-White syndrome.

This study was designed to assess the effects of isoflurane (ISO) on the electrophysiological properties of the accessory pathway, atrium, ventricle, and AV node in children with the Wolff-Parkinson-White (WPW) syndrome. The results of programmed electrical stimulation were analyzed in 51 patients (4 months to 17 years of age) with WPW. The study population was divided into two groups. Twenty-seven patients received local anesthesia and intramuscular injection of meperidine, promethazine, and chlorpromazine (MPC group). Twenty-four patients received general anesthesia with ISO inhalation (ISO group). We compared the antegrade effective refractory period of the accessory pathway (antegrade APERP), ventricular effective refractory period (VERP), atrial effective refractory period (AERP), AH interval, and cycle length of circus movement tachycardia (CMT-CL) in 12 pairs of age and sex matched patients selected from the MPC and ISO groups. Of the 12 pairs of age and sex matched patients, antegrade APERP in patients who received ISO (299 +/- 17 ms, mean +/- SEM) was significantly longer as compared with matched patients in the MPC group (262 +/- 5 ms, P < 0.025). The VERP and AERP in patients from the ISO group were significantly prolonged compared with the MPC patients (239 +/- 7 vs 210 +/- 8 ms, P < 0.025, and 228 +/- 11 vs 180 +/- 6 ms, P < 0.01, respectively). There was no significant difference in the AH interval or CMT-CL between the two subgroups. Thus, ISO prolongs the antegrade APERPs as well as the effective refractory periods of atrial and ventricular muscle in children with WPW, while the AH interval and CMT-CL appear to be unaffected. Care must be taken in interpreting measurements of the antegrade APERP made in patients under general anesthesia for RF ablation of accessory pathways.

Adjuvants, Anesthesia↗

Activation mapping of reentry around an anatomical barrier in the canine atrium: observations during the action of the class III agent, d-sotalol.

INTRODUCTION: In the chronically instrumented animal and the isolated blood perfused heart, atrial reentry via a fixed path around an anatomical obstacle has been described and is terminated by the Class III antiarrhythmic agent, d-sotalol. The precise mechanism by which d-sotalol terminates this arrhythmia is not known. METHODS AND RESULTS: In the present study, right atrial (RA) activation sequences in the isolated, coronary artery perfused canine heart during episodes of sustained flutter (n = 7) and drug administration were determined. A fixed array of bipolar electrodes was used to record endocardial electrograms from 96 sites on the RA simultaneously. Maps of all control flutters showed that the rhythm was due to persistent circus movement of the impulse around the tricuspid valve ring. D-sotalol was effective in terminating atrial reentry in this model. In all episodes, block of the excitatory impulse in a specific region of the reentrant circuit accompanied these terminations. However, the events preceding the occurrence of block of the impulse were not similar. Two different modes of termination are described. CONCLUSION: The Class III antiarrhythmic agent d-sotalol can terminate atrial reentry in several ways. In one mode, complete conduction block of the reentering impulse within the fixed path occurs to terminate the rhythm. In the other mode, interruption of the original reentrant circuit occurs when there is failure of a lateral boundary. Often in this latter case, interruption of the original circuit is by an extra impulse that is secondary to a change in the path of the impulse. In both modes cycle length oscillations are observed.

Animals↗

Endocardial mapping of reentry around an anatomical barrier in the canine right atrium: observations during the action of the Class IC agent, flecainide.

INTRODUCTION: Flecainide is effective in terminating stable atrial flutter in the conscious dog with a Y-shaped right atrial lesion. In this model, flutter is due to circus movement of the impulse around a fixed anatomical barrier. METHODS AND RESULTS: To investigate the mechanism of flecainide-induced termination of this type of reentry, we determined the pattern of endocardial activation of the right and left atria before and during administration of flecainide by recording simultaneously from 192 electrode pairs in the isolated blood perfused heart. At least five consecutive flutter beats were analyzed before and during flecainide for each of eight termination episodes in five hearts. In all, flecainide increased flutter cycle length (164 +/- 24 msec) by 89% to 309 +/- 77 msec (P < 0.05) before termination. Atrial refractory period and conduction time during paced beats were also increased by flecainide. In five episodes, termination was due to conduction block of the impulse at critical sites within the reentrant circuit (mode 1). Cycle length oscillations (+/- 30 msec) at sites proximal to site of block preceded termination in three of these episodes. In three other episodes, interruption of the original circuit occurred when there was failure of a lateral boundary, giving rise to an impulse that reset the original circuit (mode 2). In these episodes, long-short cycle length oscillations led to return reexcitation by the impulse within the primary path and subsequent termination. CONCLUSION: In summary, similar to our previous findings with the Class III agent, d-sotalol, two different modes of termination of atrial reentry were observed with flecainide.

Animals↗

Atrial flutter: historical background.

For five decades, the mechanism of atrial flutter remained controversial, with protagonists and antagonists of circus movement versus ectopic focus theories. The development of clinical electrophysiology in the 1970s and the observations made by many authors in various canine heart models supported the concept of atrial flutter as a reentrant wave confined to the right atrium. It was established that, in the common type of atrial flutter, the activation wavefront proceeds in a cranial direction over the right atrial septum and descends on the right atrial free wall in the caudal direction. A zone of slow conduction was identified inferiorly and posteriorly in the right atrium, target of the modern ablative techniques. The history of atrial flutter clearly illustrates the bidirectional flow of information and the mutual stimulation between the basic and the clinical levels, leading both to a better understanding of the nature of the arrhythmia and to new therapeutic approaches.

Animals↗

Radiofrequency ablation of a concealed nodoventricular Mahaim fiber guided by a discrete potential.

INTRODUCTION: We present the case of a 17-year-old woman who underwent an electrophysiological study and radiofrequency (RF) ablation of supraventricular tachycardia refractory to medical treatment. Two right-sided, concealed, nondecremental atrioventricular accessory pathways (AV-APs) involved in orthodromic circus movement tachycardias were identified. After RF ablation of both AV-APs, evidence of bidirectional dual AV nodal conduction was demonstrated and regular narrow complex tachycardia was induced. METHODS AND RESULTS: During the tachycardia, retrograde slow and fast AV nodal pathway conduction with second-degree ventriculoatrial (VA) block and VA dissociation were observed. During the tachycardia with second-degree VA block, ventricular extrastimuli elicited during His-bundle refractoriness advanced the next His potential or terminated the tachycardia. Mapping the right atrial mid-septal region, a distinct high-frequency activation P potential was recorded in a discrete area, two thirds of the way from the His bundle toward the os of the coronary sinus. Detailed electrophysiologic testing with the recordable P potential demonstrated that the tachycardia utilized a concealed nodoventricular AP arising from the proximal slow AV nodal pathway. CONCLUSION: The tachycardia with slow 1:1 VA conduction could be reset by ventricular extrastimuli elicited during His-bundle refractoriness advancing the subsequent activation P potential and atrial activation. RF ablation guided by recording of the activation P potential resulted in elimination of both the slow AV nodal pathway and the nodoventricular connection with preservation of the normal AV conduction system.

Adolescent↗

The role of birds as definitive hosts and intermediate hosts of heteroxenous coccidians.

Sarcocystis-like oocysts-sporocysts were found in four species of owls (Asio otus, Bubo bubo, Strix aluco, and Tyto alba) and in five species of predatory birds (Accipiter gentilis, Accipiter nisus, Buteo buteo, Circus aeruginosus, Falco tinnunculus). In addition, the muscles of 15 of 41 (36.5%) pheasants (Phasianus colchicus) and one of two jays (Garrulus glandarius) were found to harbor three types of Sarcocystis. Three of 15 (20%) infected pheasants had type I cystozoites (6-8 X 2 microns) in muscle homogenates, but sarcocysts were not seen whereas the other 12 infected pheasants had type II cystozoites (16 X 2-3 microns) and sarcocysts (90 X 600 microns) in their muscles. The one infected jay had type III cystozoites (8-10.5 X 2.5-3 microns) and sarcocysts (35-40 X greater than 770 microns) in its muscles.

Animals↗

Incessant atrial tachycardias in a dog with tricuspid dysplasia. Clinical management and electrophysiology.

In a dog, tricuspid regurgitation due to congenital tricuspid dysplasia resulted in extreme right heart enlargement and right heart failure. Incessant supraventricular tachycardias were present, requiring the intravenous administration of verapamil to reduce the ventricular rate. Oral therapy using a combination of verapamil and quinidine was partially effective in controlling the ventricular rate during the following week. At that time, electrophysiologic studies were performed. They revealed that a succession of several atrial tachycardias with different cycle lengths, including one episode of atrial flutter, was present. Atrial activity was spanning the majority of the cycle length in all these arrhythmias. Epicardial mapping was performed during the atrial flutter. This enabled the detection of a depolarization wave-front traveling counterclockwise from the dorsolateral right atrium toward the right appendage, following the tricuspid valve annulus. No areas of abnormal conduction were detected. Because programmed electric stimulation maneuvers could not be performed, definitive conclusions about the mechanism of the arrhythmia could not be drawn. The two most likely possibilities were circus movement using part of the dilated tricuspid valve annulus as an anatomic barrier or a leading circle type of re-entry.

Animals↗

Re-entrant tachycardia using two bypass tracts and excluding AV node in short PR interval, normal QRS syndrome.

In patients with the short PR interval, normal QRS complex syndrome, paroxysmal tachycardias are usually the result of circus movement involving the AV node and a partial or complete AV nodal bypass. We report 2 patients with this syndrome who suffered distressing rapid paroxysms of tachycardia but in whom there was evidence of a concealed direct VA connection. In both patients, tachycardia was initiated with critical AV prolongation distal to the His bundle, in response to programmed atrial premature stimuli. The constancy of the timing of the atrial echo from the onset of the QRS complex in the presence of a varying HV interval is evidence for involvement of the ventricles in the re-entry pathway. In addition, in both patients the appearance of left bundle-branch block during tachycardia was associated with appropriate prolongation of tachycardia cycle length consistent with the presence of a direct VA connection. The short AH interval during tachycardia and the absence of critical AH prolongation suggests the participation of a rapidly conducting pathway in the anterograde limb of the tachycardia circuit.

Adult↗

Electrophysiological effects of L 9394 (benzoyl-indolizine) in man.

The electrophysiological effects of L 9394 (benzoyl-indolizine), a substance chemically related to amiodarone, but devoid of iodine atoms, were investigated by programmed electrical stimulation of the heart in 12 patients with various forms of tachycardia. Four subjects had electrocardiographic evidence of the WPW syndrome and episodes of circus movement tachycardia. Paroxysmal supraventricular tachycardia, confined to the atrioventricular (AV) node, was found in 3 patients. In 2 cases, where a short PR interval was present, the main complaint was the occurrence of paroxysmal atrial fibrillation. In the remaining 3 instances, the arrhythmia consisted of slow ventricular tachycardia (1 case), supraventricular tachycardia of the focal type (1 case), and episodes of primary ventricular fibrillation, not related to acute myocardial ischaemia (1 case). L 9394 injected intravenously was seen to lengthen the transnodal conduction time as well as the effective and functional refractory periods of the node. Similar effects were found on the retrograde VA pathway. The drug had no action on the infra-Hisian conduction system, on the refractory periods of ventricular muscle, or on the refractory periods of accessory bypasses. The drug was injected during an episode of tachycardia in 6 cases with reproducible supraventricular re-entrant tachycardia. Three had a tachycardia circuit confined to the node. In those instances, the drug had beneficial effects (slowing and interruption of tachycardia, decrease or abolition of echo zone; loss of ability to induce tachycardia). In the other 3 cases, an accessory pathway was incorporated in the circuit. L 9394 interrupted the tachycardia in 2 instances (by anterograde AV block), but failed to protect all 3 patients against reinitiation of tachycardia by premature stimuli. It is concluded that L9394 does not share all the pharmacological properties of amiodarone and will not replace it in all its indications.

Adult↗

Slowing of paroxysmal tachycardia with loss of functional bundle-branch block.

Electrophysiological studies in a patient with paroxysmal supraventricular tachycardia disclosed anterograde dual atrioventricular nodal pathways, and a concealed left-sided anomalous atrioventricular pathway which was used as the retrograde limb of two circus movement tachycardias. Tachycardia No.1, reflecting anterograde fast pathway conduction, was characterised by functional left bundle-branch block and a stable cycle length of 330 ms. Paroxysmal loss of bundle-branch block resulted in tachycardia No.2, which reflected anterograde slow pathway conduction, and was characterised by narrow QRS and a stable cycle length of 355 ms. Tachycardia No.2 had a longer cycle length than tachycardia No.1 because the increment in AH interval (slow pathway instead of fast pathway condition) more than compensated for the decrement in ventriculoatrial interval (narrow QRS instead of bundle-branch block).

Adult↗

Recurrence rate after accessory pathway ablation.

OBJECTIVE: To evaluate characteristics of patients and accessory pathways as well as additional technical factors involved in the reappearance of accessory pathway conduction after successful ablation. DESIGN: Analysis of recurrences after radiofrequency ablation. SETTING: 163 consecutive patients with 167 accessory pathways. SUBJECTS: 97 men and 66 women with a mean (SD) age of 36 (14) range (11 to 75) years. RESULTS: After a mean (SD) follow up of 14 (7) range (2 to 27) months, conduction recurred in 13 out of 167 (7.8%) accessory pathways. The initial manifestation of recurrence was circus movement tachycardia in 7 patients and reappearance of delta waves on a 12 lead electrocardiogram in 6 patients. The interval to the return of accessory pathway conduction ranged from 3 hours to 90 days. Age, sex, presence of multiple accessory pathways, criteria to determine the target ablation site, number and duration of radiofrequency applications, and cumulative energy did not significantly differ between the groups with recurrence and without. Recurrence was less common with concealed accessory pathways (2/44) than with overt accessory pathways (11/110). The difference was not significant. The only variable to influence the recurrences in this study group was the location of the accessory pathway. Reappearance of conduction through right sided accessory pathways occurred significantly more often than through left sided ones (8/40 v 5/114, P = 0.01). CONCLUSION: After radiofrequency ablation the recurrence rate of accessory pathways is low and there are no predictors of the risk of reappearance of conduction apart from the right sided location of the accessory pathway.

Adolescent↗

Diagnosis and treatment of botulism in lions.

Six circus lions (Panthera leo) showed neurological and gastrointestinal signs after consuming casualty broiler chickens. Signs included ataxia, hindlimb paralysis and recumbency. Neurological examination of two affected males showed paralysis of extraocular muscles, fixed dilated pupils and inability to swallow. Replacement fluids and antibiotics were given and Clostridium botulinum type C antitoxin was found in serum samples. Type C antitoxin was not then available and therapy was started in one lioness with guanidine hydrochloride. Convulsions were controlled by diazepam but this animal died. One of the two males was given type C antitoxin; both were given anabolic steroids. All the remaining animals made slow recoveries over varying periods; one lion was recumbent for 41 days. No lion developed respiratory paralysis; other animals which had consumed the chickens remained healthy. Aspects of the treatment of botulism in animals are discussed.

4-Aminopyridine↗

Aujeszky's disease in captive bears.

Five of eight bears died during an outbreak of Aujeszky's disease in a travelling circus in the north of Spain. The bears had been fed on a diet which included raw pigs' heads. One of three Himalayan bears and a Kodiak bear died acutely with signs of the disease. One of four polar bears died acutely without signs, another died with signs of Aujeszky's disease while it was being treated, and a third died with enteritis and disseminated intestinal coagulation some time later without showing signs of the disease. A fourth polar bear recovered from the same gastrointestinal problem without showing signs of the disease. Although one of the two surviving Himalayan bears showed some signs referrable to Aujeszky's disease, the results of tests for neutralising antibodies were negative. Two of the polar bears, the Himalayan bear and the Kodiak bear were examined postmortem and three of them were examined histologically. No lesions referable to Aujeszky's disease were found. The tissues from one female polar bear were examined and shown to be positive for Aujeszky's disease virus by virus isolation, polymerase chain reaction, electron microscopy and fluorescent antibody tests. The DNA of the isolate was shown to be similar to that of the strains of the virus circulating in pigs in northern Spain some years earlier.

Animals↗

Vulnerability of rabbit atrium to reentry by hypoxia. Role of inhomogeneity in conduction and wavelength.

In isolated superfused left atria of the rabbit, the inducibility of tachyarrhythmias by single early premature stimuli was highly increased by hypoxia. High-resolution mapping showed that these arrhythmias were caused by circus movement around a functional arc of conduction block (leading circle reentry). To determine the electrophysiological changes by hypoxia responsible for the higher vulnerability to intra-atrial reentry, the wavelength of the atrial impulse and spatial inhomogeneities in refractory periods and local conduction delays were measured. Hypoxia caused a transient increase in refractory periods during the first 10-15 min of hypoxia. After this period, refractory periods shortened again to values slightly lower than during control. During the whole period of hypoxia, local differences in refractory periods were enlarged. Conduction velocity was significantly depressed by hypoxia. As a result, the wavelength of the atrial impulse gradually shortened during hypoxia to approximately 80% of control. Inhomogeneity in conduction was quantified by phase maps in which the maximal local delays in conduction are plotted. Hypoxia caused a marked increase in inhomogeneity in conduction both during slow rhythm (inhomogeneity index increased from 2.3 to 3.4) and premature activation (from 3.1 to 4.7). We conclude that the higher vulnerability of the atrium for reentrant arrhythmias by hypoxia is based on a combination of a moderate shortening of the wavelength and an increase in inhomogeneity in conduction of premature wavefronts.

Action Potentials↗

Gastroduodenostomy in dogs with and without parietal cell vagotomy. Effect upon gastric emptying and motility, Heidenhain pouch acid secretion and serum gastrin concentration.

Heidenhain pouch (HP) dogs were studied. After gastroduodenostomy (GD) gastric emptying time was unaffected, but cineradiography showed that the strength of the antral contractions diminished considerably, while the number of peristaltic waves increased. "Circus movements" of the barium meal through the GD to the duodenum and back to the stomach through the pylorus occurred. No significant changes in food-stimulated HP acid secretion or serum gastrin response were observed. After parietal cell vagotomy (PCV) gastric emptying and motility was unaffected, but food-stimulated HP acid secretion and serum gastrin response increased significantly. After addition of a GD to PCV gastric emptying time decreased significantly but similar changes in antral motility occurred as after GD alone. The food-stimulated HP acid secretion and serum gastrin response became significantly reduced. Fasting HP acid secretion and serum gastrin concentration were not significantly altered by any of the surgical procedures.

Animals↗