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Bread and circuses.

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Community Health Services↗

A circus atmosphere.

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Complementary Therapies↗

Atrial activation sequence during atrial flutter in the canine pericarditis model and its effects on the polarity of the flutter wave in the electrocardiogram.

Stable atrial flutter induced in both conscious and open chest states was studied in 30 mongrel dogs after production of sterile pericarditis. During the conscious state studies, induced atrial flutter (mean cycle length 128 +/- 15 ms) was always sustained greater than 15 min and was stable. Three types of flutter wave polarity were noted in electrocardiogram (ECG) lead II: positive in 16 dogs, negative in 3 and flat or slightly positive in 11. Sequential site atrial mapping during atrial flutter (mean cycle length 133 +/- 18 ms) in the open chest state showed either clockwise (18 dogs) or counterclockwise (12 dogs) circus movement in the right atrium. In 19 of 30 dogs, the circus movement clearly did not require any naturally existing anatomic obstacle; in 11, the orifice of the superior vena cava probably was also involved. Double potentials were recorded from the center of the reentrant circuit during atrial flutter, and fractionated electrograms were recorded from a pivot point of the reentrant wave front. A positive flutter wave in ECG lead II (12 dogs with counterclockwise circus movement) was associated with early activation of the Bachmann's bundle region compared with the posteroinferior left atrium and activation of the left atrium mainly in a superoinferior direction. A negative flutter was associated with the early activation of the posteroinferior left atrium compared with Bachmann's bundle and activation of a considerable portion of the left atrium in an inferosuperior direction. A flat or slightly positive flutter wave (14 of 18 with clockwise circus movement) was associated with activation of the left atrium almost simultaneously by two wave fronts coming from both these sites. In conclusion, atrial flutter in this dog model is due to circus movement in the right atrium, the center of which does not necessarily require an anatomic obstacle. Although atrial flutter is generated by circus movement in the right atrium, the flutter wave polarity in the ECG is determined primarily by the activation sequence of the left atrium.

Animals↗

Localization of the accessory pathway in the Wolff-Parkinson-White syndrome from the ventriculo-atrial conduction time of right ventricular apical extrasystoles.

In 18 consecutive patients with the Wolff-Parkinson-White syndrome undergoing electrophysiologic study, the ventriculo-atrial conduction time of right ventricular apical extrasystoles which advanced atrial activation during circus movement tachycardia was studied in relation to accessory pathway location. Accessory pathway location was determined by delta wave morphology during maximal pre-excitation, mapping of atrial activation during circus movement tachycardia and ventricular pacing, the effect of bundle branch block on ventriculo-atrial conduction time during circus movement tachycardia, and the effect of pacing from different sites in the atria on the stimulus-to-delta wave interval. In 7 patients with septal accessory pathways, ventriculo-atrial conduction time was similar during circus movement tachycardia and following right ventricular apical extrasystoles (mean difference 0 +/- 6 ms, range -5 to +10 ms). In contrast, in 11 patients with a left free wall accessory pathway, ventriculo-atrial conduction time increased by 46 +/- 15 ms (range 15 to 65 ms) following right ventricular apical extrasystoles. Therefore, measurement of the ventriculo-atrial conduction time of right ventricular extrasystoles during circus movement tachycardia provides an easy way to distinguish between septal and left free wall accessory pathways. This finding may be of particular use in determining the location of concealed bypass tracts.

Adolescent↗

Properties of ectopic neurons induced by Xenopus neurogenin1 misexpression.

We have examined cells cultured from ectoderm-misexpressing Neurogenin1 (Ngn1) to describe better the extent to which this gene can control aspects of neuronal phenotype including motility, morphology, excitability, and synaptic properties. Like primary spinal neurons which normally express Ngn1, cells in Ngn1-misexpressing cultures exhibit a motility-correlated behavior called circus movements prior to neuritogenesis. Misexpression of NeuroD also causes circus movements and later neuronal differentiation. GSK3beta, which inhibits NeuroD function in vivo, blocks both Ngn1-induced and NeuroD-induced neuronal differentiation, while Notch signaling inhibits only Ngn1-induced neuronal differentiation, confirming that NeuroD is downstream of Ngn1 and insensitive to Notch inhibition. While interfering with NeuroD function in ventral ectoderm inhibits both circus movements and neuronal differentiation, such inhibition in the neural plate inhibits only neuronal differentiation, suggesting that additional factors regulate circus movements in the neural ectoderm. Ngn1-misexpressing cells extend N-tubulin-positive neurites and exhibit tetrodotoxin-sensitive action potentials. Unlike the majority of cultured spinal neurons, however, Ngn1-misexpressing cells do not respond to glutamate and do not form functional synapses with myocytes, suggesting that these cells are either like Rohon-Beard sensory neurons or are not fully differentiated.

Animals↗

Reentry in the atrium.

Studies with isolated atrial preparations of the rabbit showed that the occurrence of a single early premature beat may cause reentry not only in nodal tissue (SA node and AV node) but also in working myocardial tissue. In the SA node an early premature beat will cause a reentrant activation of the atrium only when the SA node is driven by an ectopic pacemaker. If the SA node is discharging spontaneously, no reentry could be demonstrated. In this situation the early impulse can not reach the center of the SA node because of a sinoatrial entrance block. Since the AV node fibers normally do not discharge spontaneously, an atrial premature beat may find an alternative route through the node and reenter the atrium. Such a reentrant beat or echo beat can start a tachycardia based on a circus movement of the impulse through the AV node. A supraventricular tachycardia can be started too by an early premature beat in the isolated left atrium, containing only working myocardial fibers and no slow conducting fibers as the nodal fibers are. By careful mapping the spread of activation during the premature beat and the subsequent beats of the tachycardia, a unidirectional block of the impulse of the premature beat was demonstrated. The impulse then turned around and invaded the blocked area retrogradely and reentered the area where it originated. This circus movement of the premature impulse was maintained during the subsequent tachycardial beats, showing that even in a small area of atrial muscle, containing no anatomical obstacle, a circus tachycardia can take place. To describe this kind of circus movement a new model (the "leading circle" concept) is introduced and briefly discussed.

Atrial Function↗

[Induction of atrial fibrillation by adenosine in a patient with supraventricular tachycardia].

Adenosine is generally considered to be safe and effective in treatment of orthodromic circus movement tachycardia in patients with accessory pathways. We present a case with reproducible induction of atrial fibrillation after initial successful termination of orthodromic circus movement tachycardia using a left sided accessory pathway by adenosine. With the induction of atrial fibrillation sudden onset of preexcitation with subsequent rapid ventricular response was accompanied by moderate hemodynamic compromise. Before and after successful ablation of the accessory pathway, adenosine was not able to induce atrial fibrillation when applied during sinus rhythm. Adenosine induced atrial fibrillation is due to shortening of the atrial action potential duration and atrial refractoriness, whereas shortening of the antegrade refractory period in the accessory pathway leads to rapid conduction to the ventricles. Thus, care should be taken using adenosine in patients with orthodromic circus movement tachycardias and evidence of antegrade preexcitation during sinus rhythm.

Adenosine↗

Effect of amiodarone in the Wolff-Parkinson-White syndrome.

The effect of amiodarone in the Wolff-Parkinson-White syndrome was studied with programmed electrical stimulation of the heart in 15 patients. All 15 patients had circus movement tachycardias; 7 also had atrial fibrillation. Programmed electrical stimulation was performed before and after 14 days of oral administration of amiodarone. The effective refractory period of the accessory pathway lengthened in an atrioventricular direction in all patients and in a ventriculoatrial direction in eight patients. The effective refractory period of the atrium and ventricle lengthened in 14 and 12 patients, respectively. After administration of amiodarone, circus movement tachycardia could no longer be initiated in five patients. The zone of tachycardia narrowed in four patients, did not change in two and increased in seven. The effect of amiodarone on initiation of circus movement tachycardia could be related to differences in effect of the drug and in the mechanism of tachycardia in individual patients. In all patients in whom tachycardias could still be initiated after treatment with amiodarone the heart rate during tachycardia was slower than before treatment. This slowing was caused by a decrease in conduction velocity of the circulatory wave in different parts of the tachycardia circuit. The effect of amiodarone in prolonging the refractory period of the accessory pathway makes this drug especially useful in patients with the Wolff-Parkinson-White syndrome and atrial fibrillation.

Adolescent↗