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Impulse propagation at the septal and commissural junctions of crayfish lateral giant axons.

Transmission across the septal junctions of the segmented giant axons of crayfish is accounted for quantitatively by a simple equivalent circuit. The septal membranes are passive, resistive components and transmission is ephaptic, by the electrotonic spread of the action current of the pre-septal spike. The electrotonic spread appears as a septal potential, considerably smaller than the pre-septal spike, but usually still large enough to initiate a new spike in the post-septal segments. The septal membranes do not exhibit rectification, at least over a range of +/- 25 mv polarization and this accounts for their capacity for bidirectional transmission. The commissural branches, which are put forth by each lateral axon, make functional connections between the two axons. Transmission across these junctions can also be bidirectional and is probably also ephaptic. Under various conditions, the ladder-like network of cross-connections formed by the commissural junctions can give rise to circus propagation of impulses from one axon to the other. This can give rise to reverberatory activity of both axons at frequencies as high as 400/sec.

Animals↗

Multiple modes of termination of re-entrant excitation around an anatomic barrier in the canine atrium during the action of d-sotalol.

In the chronically-instrumented animal and the isolated blood perfused heart, atrial re-entry via a fixed path around an anatomic 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. In the present study, right atrial (RA) activation sequences in the isolated, coronary artery perfused canine heart (n = 5) during episodes of sustained flutter 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 re-entry in this model. In all episodes, block of the excitatory impulse in a specific region of the re-entrant 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. The class III antiarrhythmic agent d-sotalol can terminate atrial re-entry in several ways. In one mode, complete conduction block of the re-entering impulse within the fixed path occurs to terminate the rhythm. In the other mode, interruption of the original re-entrant circuit occurs when there is failure of a lateral boundary. In both modes cycle length (CL) oscillations are observed.

Animals↗

One-year follow-up in a prospective, randomized study comparing radiofrequency and cryoablation of arrhythmias in Koch's triangle: clinical symptoms and event recording.

AIMS: To rely solely on clinical symptoms of recurrent palpitations to evaluate the success of interventional procedures can be misleading. This study was designed to assess the efficacy of event recording in evaluating long-term success in patients treated for atrioventricular nodal reentrant tachycardia (AVNRT) or right posteroseptally located accessory pathways (RPS) either by radiofrequency (RF) or by cryoablation (CA). METHODS AND RESULTS: Sixty-three patients with AVNRT and eight with RPS were randomized. Patients were encouraged to activate an event recorder in the case of recurrent palpitations for the first 3 months. One year after the procedure, patients were asked specific arrhythmia related questions. Thirty-six patients underwent RF and 35 CA. Acute success was finally achieved in 34 (94%) patients in the RF and 33 (94%) in the CA groups. Assessment of long-term success demonstrated a similar proportion of palpitations in the RF and CA groups: 11 (31%) vs. 17 (49%). Only 12 patients activated the event recorder, four patients in RF, including one patient with chest pain, and eight in the CA group. Analysis of recordings revealed recurrent AVNRT or circus movement tachycardia in four patients (one RF and three CA), atrial fibrillation in one RF patient, and sinus tachycardia in six (one RF and five with CA). In addition, a complete 12 lead ECG of a recurrent arrhythmia was made in three RF and two CA patients (in-hospital or after the event recording). A total of seven patients underwent a second procedure (four RF and three CA). Without the event recorder, seven patients would have been misclassified as having recurrent arrhythmia. CONCLUSION: Event recording enhances the sensitivity of detecting arrhythmia recurrences in evaluating therapy efficacy and should be considered in every interventional follow-up study. Analysis of recordings showed that CA is as effective as RF in the treatment of AVNRT and RPS at long-term follow-up.

Arrhythmias, Cardiac↗

Mechanisms of termination of supraventricular tachycardias by intravenous class III antiarrhythmic agents. A comparison of amiodarone and sotalol.

The effects of amiodarone and sotalol were studied with programmed electrical stimulation of the heart in 19 patients with inducible tachycardia (AV nodal tachycardia: 10 cases, circus movement tachycardia: 9 cases). Amiodarone was administered intravenously at a dose of 300 mg over 2 min and sotalol at a dose of 1.5 mg kg-1 over 10 min. Both i.v. amiodarone and sotalol lengthened the transnodal conduction time, the effective refractory period of the AV node and the AV nodal Wenckebach cycle length. Only sotalol significantly lengthened the effective refractory periods of the right atrium and the right ventricle. Infused intravenously during tachycardia, amiodarone interrupted arrhythmia in five of six patients and sotalol in seven of ten cases. Tachycardia was stopped by blockade of the impulse into the AV node in three amiodarone patients and in five sotalol patients. In the remaining four cases, the weak link of the circuit was the accessory pathway. Thus i.v. sotalol exhibits electrophysiologic effects consistent with both class II and III activity, whereas the effects of i.v. amiodarone are the result of different activities throughout all areas of the cardiac tissue.

Adolescent↗

Effects of intravenous diltiazem administration in patients with inducible tachycardia.

The efficacy of diltiazem was studied with programmed electrical stimulation of the heart in 13 patients with inducible tachycardia (atrioventricular nodal tachycardia: 8 cases; orthodromic circus movement tachycardia involving an accessory pathway: 4 cases; ventricular tachycardia: one case). Diltiazem was administered intravenously at a dose of 0.25 mg kg-1 over 2 min. It lengthened the transnodal conduction time, and the effective and the functional refractory periods of the AV node. The shortest pacing cycle length with 1:1 conduction through the node lengthened both in the anterograde and retrograde directions. Diltiazem did not alter anterograde or retrograde refractoriness of accessory pathways. Infused intravenously during episodes of tachycardia, diltiazem interrupted the arrhythmia in all patients. Tachycardia could still be initiated in 2 patients after drug, but the arrhythmia was not sustained in one case. One patient with preexcitation and atrial fibrillation exhibited an increase in ventricular rate after diltiazem. The shortest RR intervals before and after diltiazem were 240 ms and 180 ms, respectively. Thus, iv diltiazem is an effective antiarrhythmic drug for patients with reciprocal supraventricular tachycardia and for selected patients with ventricular tachycardia.

Adolescent↗

Sudden death in a young competitive athlete with Wolff-Parkinson-White syndrome.

The case history is documented of a young competitive athlete known to have the electrocardiographic pattern of the Wolff-Parkinson-White syndrome, but considered asymptomatic. On that basis competitive sport was not proscribed. In retrospect, he had experienced occasional tachycardias which were of short duration and ended spontaneously. He never requested medical advice. The boy was first admitted for an attack of rapid heart beating which did not readily subside. He was medicated with prajmalium and left the hospital in stable condition. He died suddenly 10 days after discharge. Autopsy examination of the heart revealed an accessory atrioventricular connection in the posterior septal region. The case history underlines that in some patients with the Wolff-Parkinson-White syndrome the clinical manifestation can be minimal and may be easily ignored by the patient. In retrospect, benign episodes of rapid heart beating most likely were due to a circus movement tachycardia, related to an accessory atrioventricular connection. The sudden death can be attributed to atrial fibrillation with rapid ventricular response via the anomalous connection, despite medical treatment. The observation endorses the potential danger of the Wolff-Parkinson-White syndrome in patients with minimal clinical manifestations. A meticulous histologic study of the atrioventricular junction in hearts of young athletes with sudden and unexplained death is a necessity.

Adolescent↗

Ion channels and ventricular arrhythmias: cellular and ionic mechanisms underlying the Brugada syndrome.

Brugada syndrome is characterized by ST segment elevation in the right precordial leads, V1-V3 (unrelated to ischemia or structural disease), normal QT intervals, apparent right bundle branch block, and sudden cardiac death, particularly in men of Asian origin. An autosomal dominant mode of inheritance with variable expression has been described. The only gene thus far linked to the Brugada syndrome is the cardiac sodium channel gene, SCN5A. The possible cellular and ionic basis for these features of the Brugada syndrome are discussed. Strong sodium channel block, among other modalities, has been shown to be capable of inducing epicardial and transmural dispersion of repolarization, thus providing the substrate for the development of phase 2 and circus movement reentry, which underlies ventricular tachycardia/ventricular fibrillation.

Animals↗

Class III antiarrhythmic action in experimental atrial fibrillation and flutter in dogs.

Progress in the pharmacological treatment of atrial fibrillation and flutter has been achieved by the introduction of the class III antiarrhythmic drug amiodarone. In the present study we tested amiodarone and a new class III antiarrhythmic drug, melperone, in experimentally induced atrial fibrillation and flutter in pentobarbital-anesthetized dogs. By high-rate stimulation in the right atrium, atrial fibrillation was induced in 4, and atrial flutter in 10 out of 22 dogs. Atrial flutter rate was 496 +/- 13 min-1 (median +/- 95% confidence interval). Both drugs converted the arrhythmias at doses from 2.5 to 10 mg . kg-1 and reduced that atrial flutter rate before conversion. Average ventricular rate during arrhythmias (261 +/- 16 min-1) decreased after amiodarone, and was unchanged or, in three out of nine dogs, increased after melperone. The doses of amiodarone converting the arrhythmias increased atrial refractoriness, whereas the effects on AV nodal conduction and refractoriness were variable. The results support the concept that atrial flutter is due to circus movement where the flutter rate is dependent upon atrial refractoriness. The class III antiarrhythmic drugs amiodarone and melperone seem to be equally potent in converting atrial arrhythmias.

Amiodarone↗

Electrophysiological actions of amrinone in dogs with cardiac lesions.

We examined the actions of amrinone in five models using dogs to determine under what circumstances intravenous amrinone might exert arrhythmogenic or antiarrhythmic properties. In dogs with 24-h post-coronary artery ligation arrhythmias, amrinone, given at incrementally increasing doses of 1.5, 3.0, and 6.0 mg/kg at 30-min intervals, produced significant increases of cardiac contractility without altering the severity of the arrhythmia. In dogs with 2- to 6-day-old ischemic lesions and 90-100% sinus beats, a bolus dose of 3.0 mg/kg amrinone was followed by an increased incidence of abnormal beats (p = 0.013); neither 1.5 nor 6.0 mg/kg caused a significant incidence of arrhythmias. Acute occlusion of the left anterior descending coronary artery followed by reperfusion caused fibrillation in nine of 15 control dogs and two of 14 dogs treated with 2.3 mg/kg amrinone. This difference was significant at the level p less than 0.05. In ouabain-intoxicated dogs, amrinone at 1.0 and 3.0 mg/kg neither worsened nor improved the arrhythmias. In the atrial circus flutter arrhythmia, amrinone increased ventricular heart rate by a significantly greater amount than it increased atrial rate, suggesting that amrinone facilitates atrioventricular conduction.

Aminopyridines↗

Electrophysiologic effects of an acute beta-blockade induced by bisoprolol in patients with supraventricular tachycardia as assessed by His-bundle electrograms.

The acute electrophysiologic effects of 10 mg bisoprolol (B, given intravenously) were evaluated during an electrophysiological study in 10 patients with a history of paroxysmal tachycardia. Drug administration resulted in a significant decrease of sinus rate (Control [C]; 70.8/min; B: 59.4), and in an increase in sinus node recovery time (+20%). AV-nodal depression was marked at high heart rates during incremental atrial pacing. A second-degree AV-block occurred at a pacing cycle length (CL) of 329 ms (182/min) before and at a CL of 378 ms (158/min) after drug administration. Depression of AV-nodal conduction was negligible at low heart rates; the AH-interval at sinus rhythm was not affected (C: 84 ms, B: 86 ms); and functional and effective refractory periods of the AV-node were only slightly prolonged. Conduction intervals and refractory periods on atrial and ventricular level did not change. In 5 of 6 patients with accessory AV-pathways, circus movement tachycardia (CMT) could be elicited prior to as well as after B. Due to AV-nodal delay, CMT CL was slightly prolonged after B. Echozone and refractoriness of accessory pathways were not affected. In 1 of 2 patients with ectopic atrial tachycardia, B prevented the induction of paroxysms. In one patient with paroxysmal atrial fibrillation, the ventricular response decreased from 128/min to 94/min. The findings suggest that the electrophysiologic effects of B are due to a selective beta-adrenergic antagonism. Therapeutic efficacy is only to be expected if an increased adrenergic drive is a prerequisite for induction and continuation of a tachycardia.

Adrenergic beta-Antagonists↗

Relationship between an arrhythmogenic action of lidocaine and its effects on excitation patterns in acutely ischemic porcine myocardium.

To investigate the relationship between the effects of lidocaine on excitation patterns and its effects on the incidence of arrhythmias, the left anterior descending coronary artery was occluded for 6-min periods separated by 30 min of reperfusion, under control conditions and after injection of lidocaine, at a dose of either 2.5, 5.0, or 10.0 mg/kg i.v., in 29 open-chest anesthetized pigs. Sixty-three unipolar electrograms and a surface lead electrocardiogram were continuously recorded during atrial pacing and spontaneous ventricular arrhythmias. Ventricular fibrillation (VF) occurred only in four of a total of 45 control occlusions. VF occurred in two of five pigs following injection of lidocaine 2.5 mg/kg, in 15 or 17 pigs following injection of a 5 mg/kg dose, and in all three preparations following injection of a 10 mg/kg dose. Just prior to VF during occlusions preceded by injections of lidocaine 5 mg/kg, activation time of ischemic myocardium in atrial-paced beats was delayed by only 30 +/- 17 ms beyond preocclusion values, compared with 18 +/- 11 ms at a similar time during control occlusions and 33 +/- 18 ms at the end of control occlusions (mean +/- SD; n = 8). As ventricular tachycardia (VT) developed in the presence of lidocaine, conduction was further slowed or blocked in ischemic areas, and slowed in nonischemic regions; at the transition from VT to VF, excitation patterns displayed circus movement involving nonischemic regions.

Animals↗

Electrophysiological effects of a new antiarrhythmic agent, nicainoprol, in humans.

The electrophysiological effects of nicainoprol, a new antiarrhythmic drug, were evaluated in a heterogeneous group of 23 patients aged 59 +/- 15 (mean +/- standard deviation) years. Nicainoprol was administered intravenously as a bolus of 1-2 mg/kg followed by continuous infusion at two dose levels. Electrophysiologic study was performed before and during the infusion at a steady-state drug level on each dose. The sinus node recovery time was unaltered in patients with normal sinus node function and was markedly prolonged in three of six patients with sinus node dysfunction. The intranodal conduction time (p less than 0.01) and the infranodal conduction time (p less than 0.001) increased, and the QRS duration (p less than 0.05) lengthened significantly even during 1 mg/kg/h. During 2 mg/kg/h, these times were further prolonged and, in addition, the intra-atrial conduction time (p less than 0.05), atrioventricular nodal effective and functional refractory periods (p less than 0.01), as well as the Wenckebach cycle length (p less than 0.001) also increased significantly. Similar depressant effects on the retrograde ventriculoatrial conduction system were also produced by nicainoprol. Retrograde His-atrioventricular nodal conduction was blocked in six of eight patients with this condition and was prolonged in the remaining two. Sustained supraventricular tachycardia was induced in seven patients, five of whom received nicainoprol during the tachycardia. The termination of supraventricular tachycardia was exclusively due to ventriculoatrial block in all five subjects, three with orthodromic circus movement tachycardia and two with atrioventricular nodal reentrant tachycardia of the slow-fast type. The reinducibility of supraventricular tachycardia could be prevented in five of seven patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Law's effect on the quality of end-of-life care: lessons from the Schiavo case.

The political circus surrounding Terri Schiavo's death is unlikely to repeat itself soon in other cases but the underlying event that precipitated the furor is a recurrent clinical problem-the problem of conflict among family members about withdrawing or withholding life-prolonging treatment for an incompetent patient who had left no advance directive or appointed healthcare proxy. The laws of most states purport to solve this problem by automatic appointment of one person among the disputing family members. However, this forced resolution of the family conflict does not clearly reflect the prior values of the incompetent patient and is likely to intensify rather than ease that conflict, providing no demonstrable benefit to the incompetent patient and complicating the psychological processes of mourning for the surviving family. This article explores the benefits of a different legal rule that would require family consensus before life-prolonging treatment is withdrawn or withheld for an incompetent patient who has indicated no prior wishes regarding the resolution of family conflict.

Advance Directives↗

Ultraviolet reflectance by the cere of raptors.

Ultraviolet (UV) signals have been shown to play key roles in social and sexual signalling in birds. Using a spectrophotometer, we analysed the colour of the cere (skin above the beak) of a diurnal raptor, the Montagu's harrier (Circus pygargus), and show that it reflects in the UV part of the spectrum. The cere is a well-known sexual signal in raptors, with carotenoid based pigmentation being indicative of quality. We thus hypothesized that UV reflectance also signals quality. Accordingly, we found that in our sample of wild males, the location of the UV peak was related to the orangeness of cere and correlated with male body mass and condition (mass corrected for size). Also, males with brighter UV were mated to females that laid earlier, as expected if UV reflectance relates to a male's quality and attractiveness. Future studies should investigate the relationships between UV reflectance and carotenoid pigmentation of cere, and test how UV reflectance influences mate choice.

Animals↗

Habitat loss and raptor predation: disentangling long- and short-term causes of red grouse declines.

The number of red grouse (Lagopus lagopus scoticus) shot in the UK has declined by 50% during the 20th century This decline has coincided with reductions in the area of suitable habitat and recoveries in the populations of some avian predators. Here we use long-term records of shooting bags and a large-scale manipulation of raptor density to disentangle the effects of habitat loss and raptor predation on grouse populations. The numbers of grouse harvested on the Eskdale half of Langholm Moor in southern Scotland declined significantly during 1913-1990 and grouse bags from the whole moor from 1950 to 1990 exhibited an almost identical but non-significant trend. Hen harriers (Circus cyaneus) and peregrine falcons (Falco peregrinus) were absent or bred at low densities on this moor throughout this period but heather-dominant vegetation declined by 48% between 1948 and 1988. Harrier and peregrine breeding numbers on Langholm Moor increased to high levels following protection in 1990 whilst grouse density and grouse bags declined year after year until shooting was abandoned in 1998. The prediction of a peak in grouse bags on Langholm Moor in 1996 based on the patterns of bags during 1950-1990 was supported by the observed peaks in 1997 on two nearby moors with few raptors which formerly cycled in synchrony with Langholm Moor. This study demonstrates that, whilst long-term declines in grouse bags were most probably due to habitat loss, high levels of raptor predation subsequently limited the grouse population and suppressed a cycle. This study thus offers support to theoretical models which predict that generalist predators may suppress cycles in prey populations.

Animals↗

Neurofibromatosis: relinquishing the masks; a quest for quality of life.

Neurofibromatosis (NF) or von Recklinghausen's disease is mankind's most common neurologic genetic disorder, occurring in one of every 3000 live births. While many individuals with NF suffer disfiguring, disabling, or life-threatening complications, NF is extremely variable in its symptoms, intensity, and progression. For many of its victims, NF is a pseudonym for uncertainty and physical and psychosocial havoc. John Merrick, 'The Elephant Man', endured one of the most severe cases of NF ever recorded. Merrick's rejection by post-Dickensian England forced him to become a sideshow circus attraction just to survive. The essence of nursing intervention with NF patients and their families engaged in the quest for quality of life is to restore them to optimal physical and psychosocial functioning, and, ideally, to help them utilize the experience for growth. Many individuals respond to the frustration of NF and society's reactions to the disorder by the wearing of psychological masks. Likewise, nurses may wear emotional masks as a defence against their own discomfort and fears concerning the disorders. Comprehensive nursing management of NF is realized only as nurses and patients relinquish their respective masks. This article examines the nurse's role in genetic disorders with special considerations presented by NF. Adaptation to NF involves coping with NF and its accompanying sequelae and coping with life as it is affected by NF. The concepts of 'chromosomal coping', 'genetophobia', 'genetic guilt, and 'genetic overload syndrome' are presented and analyzed utilizing the theoretical nursing frameworks of Imogene King and Sister Callista Roy.

Adaptation, Psychological↗

A dual model for cardiac arrhythmias: coexistence of re-entry and abnormal automaticity and effects of antiarrhythmic agents.

1. We have developed a dual model for arrhythmia anaesthetized dogs. The model consists of an inducible re-entrant atrial tachycardia and spontaneous ventricular ectopies in the same heart. 2. The model for re-entrant atrial tachycardia was created by crushing the right atrium longitudinally in the intercaval region and transversely in the front free wall parallel to the atrioventricular groove. Ventricular abnormal automaticity was produced by prior (20 approximately 24 h) left anterior descending coronary artery occlusion. The ventricular arrhythmia was partially suppressed during rapid pacing-induced atrial tachycardia and resumed after atrial re-entry was terminated. 3. Mapping experiments indicate that the atrial tachycardia was due to circus movement occurring in the tissue around the tricuspid ring. This re-entrant circuit was identical to that induced in the model created by the incision method. 4. Clofilium (0.75 mg kg-1, n = 5) increased the cycle length of atrial re-entry by 14 +/- 4% from 139 +/- 12 to 159 +/- 18 ms (P less than 0.05). Flecainide (1.8 +/- 0.9 mg kg-1, n = 5) prolonged the cycle length of the tachycardia by 114 +/- 57% from 158 +/- 11 to 332 +/- 66 ms (P less than 0.05). 5. Both drugs terminated the atrial arrhythmia, but re-entry could be reinduced only in flecainide-treated dogs. Flecainide reduced ventricular ectopies by 89 +/- 19%, whereas clofilium did not change ventricular abnormal automaticity or maximum pacing cycle length that is necessary to overdrive the ventricle fully. 6. These data indicate that the dual model provides coexisting arrhythmias of different mechanisms in the same heart and that Class I and Class III anti-arrhythmic drugs may be differentiated from each other by the distinct patterns of pharmacological activities produced in this test system.

Animals↗

Pacemaker related tachycardias.

Three cases of pacemaker interactive tachycardia are presented. The first two are [artificial] circus movement tachycardias. In the first one the retrograde arm of the tachycardia circuit was provided by the A-V node and the antegrade arm by an atrial synchronous pulse generator. In the second case, the A-V node and, coincidentally, an A-V sequential pulse generator alternately provided the antegrade arm while the retrograde arm was by way of an accessory pathway. In the third case ventricular inhibition during A-V sequential pacing gave the paced atrial events the chance to be conducted to the ventricles with a long A-V interval. This resulted in a tachycardia with a rate of 150 bpm, instead of the programmed rate of 110 bpm.

Adult↗