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PubMed1976

Tachycardias and electrical pacing.

Techniques of electrical pacing for the treatment of tachycardias are multiple. The choice of a suitable method for a particular tachycardia depends upon understanding the mechanism of the tachycardia and the pacing characteristics that will lead to interruption or suppression of the tachycardia, or to ventricular slowing. Electrical pacing is indicated for tachycardias when drug therapy alone has failed or cannot be initiated or continued, and only for those tachycardias that are likely to respond to this type of electrical stimulation. In either the circus movement type or the ectopic pacemaker type an ectopic tachycardia is more likely to be suppressed if the pacing site is near the site of origin of the tachycardia. Pacing more rapidly than the basic rate in order to prevent or abolish tachycardias is termed overdrive suppression. The mechanisms responsible for this phenomenon may be associated with release of acetylcholine, release of potassium, activation of an electrogenic sodium pump, increase in cardiac output and coronary flow, decrease in size of the heart with a consequent decrease in wall tension, and decrease in the inhomogeneity of recovery of excitability that occurs at more rapid rates in the non-ischemic heart. All of these effects of pacing suppress accelerated pacemaker activity or prevent emergence of conditions favorable for development of circus movement tachycardias. Paired, coupled, or rapid atrial pacing may improve ventricular performance or slow ventricular rate, or both, without abolishing the ectopic pacemaker activity. Atrial pacing with pacing sites located at endocardial, epicardial, coronary sinus, trans-septal, or esophageal locations may interrupt or prevent rapid supraventricular or ventricular arrhythmias. Similarly, ventricular pacing at endocardial, epicardial, myocardial, or transthoracic sites may be equally effective. Artificial pacing has abolished almost every type of tachycardia. Ventricular fibrillation always, and atrial fibrillation usually, require countershock if electrical treatment is to be employed, although defibrillation of the atria by rapid pacing has been reported once. Unipolar or bipolar pacemakers may be used temporarily, or permanently after implantation. Pacing rates used to abolish supraventricular tachycardias range from single premature beats to alternating current atrial pacing at 3600 cycles per minute. Artificial electrical stimulation of the heart may be on demand, or may be competitive (fixed rate). External magnets, induction coil coupling, and radio frequency signals allow competitive pacing to be used intermittently, with permanently implanted pacemakers. Thus, electrical pacing of the heart is a technique of major importance for the control of rapid heart rates.

Action Potentials↗
PubMed1987

High frequency alternating current ablation of an accessory pathway in humans.

High frequency alternating current ablation of an accessory pathway was performed in a patient with incessant circus movement tachycardia using a right-sided, free wall accessory pathway. Antiarrhythmic drugs, antitachycardia pacing and transvenous catheter ablation using high energy direct current shocks could not control the supraventricular tachycardia. A 7F bipolar electrode catheter with an interelectrode distance of 1.2 cm was positioned at the site of earliest retrograde activation during circus movement tachycardia. At this area, two alternating current high frequency impulses were delivered with an energy output of 50 W through the distal tip of the bipolar catheter, while the patient was awake. After the first shock supraventricular tachycardia terminated and accessory pathway conduction was absent without altering anterograde conduction in the normal atrioventricular (AV) conduction system. No reports of pain or other complications were noted. In short-term follow-up of 5 months, the patient had been free of arrhythmias without antiarrhythmic medication. Thus, high frequency alternating current ablation was performed for the first time in the treatment of an arrhythmia incorporating an accessory pathway in a human. This technique may be an attractive alternative to the available transcatheter ablation techniques and to antitachycardia surgery.

Adult↗
PubMed1984

Occurrence of Leucocytozoon and Haemoproteus (Apicomplexa, Haemosporina) in Falconiformes and Strigiformes of Italy.

Blood smears from Falconiformes (91 birds of 10 species) and Strigiformes (23 birds of 5 species) captured in Italy, were examined for haematozoa. Leucocytozoon were found in Falco tinnuculus, Buteo buteo, Circus cyaneus, Circus pygargus, Accipiter nisus from Falconiformes and in Strix aluco, from Strigiformes. Haemoproteus were found in Falco tinnuculus and Strix aluco; this latter species harbored mixed infections Leucocytozoon-Haemoproteus. Prevalences were 20.80% in Falconiformes and 21.74% in Strigiformes.

Animals↗
PubMed1983

Effects of flecainide on electrophysiological properties of accessory pathways in the Wolff-Parkinson-White syndrome.

The effect of flecainide in 12 patients with the Wolff-Parkinson-White syndrome was analyzed with respect to the anterograde and retrograde conduction properties of the accessory pathway, the modes of initiation and termination of circus movement tachycardias, and the ventricular response during induced atrial fibrillation. The principal effect of this drug was to depress both anterograde and retrograde conduction of the accessory pathway. In 8/9 cases circus movement tachycardia was terminated by prolongation of the retrograde effective refractory period of the accessory pathway. Flecainide increased the shortest and the mean cycle length during induced atrial fibrillation. It is concluded that the drug may be of potential benefit in patients with paroxysmal supraventricular tachycardias in patients with the Wolff-Parkinson-White syndrome.

Adult↗
PubMed1985

Electrophysiologic effects, antiarrhythmic activity and pharmacokinetics of cibenzoline studied with programmed stimulation of the heart in patients with supraventricular reentrant tachycardias.

Cibenzoline, an imidazoline derivative is a new antiarrhythmic agent. Its electrophysiological effects and antiarrhythmic properties were studied with programmed electrical stimulation of the heart in 12 patients with recurrent episodes of reentrant supraventricular tachycardia; atrionodal (5 cases), circus movement tachycardia involving an accessory pathway (6 cases), intraatrial reentry (one case). Cibenzoline was infused intravenously at a dose of 1 mg kg-1 to 1.75 mg kg-1 during sustained episodes of tachycardia and over 9 to 15 min. Cibenzoline shortened the sinus cycle length, moderately increased the transnodal conduction time and markedly lengthened the HV interval. The refractory periods of the atrioventricular (A-V) node, the atrium and the ventricle did not change. The effects of cibenzoline on accessory pathways used in the anterograde direction were measurable in 4 cases. Complete blockade of the bypass was seen in every case. In the retrograde direction the refractory period of the bypass could be evaluated; in 5 patients it lengthened systematically. Infused intravenously during epidoses of tachycardia, the drug terminated the rhythm disorder in 9 out of 12 cases. Tachycardia could still be initiated in 8 patients after i.v. cibenzoline (2 out of 5 A-V nodal tachycardias, 6 out of 6 circus movement tachycardias). The distribution of the drug followed a bicompartment pharmacokinetic model. The plasma levels at the end of infusion ranged from 1.34 to 3.19 microgram ml-1. Cibenzoline, primarily has class I antiarrhythmic properties and its well-understood pharmacokinetics should be of help in tailoring the treatment to the individual needs of the patient.

Adolescent↗
PubMed2001

Basic mechanisms of reentrant arrhythmias.

The mechanisms responsible for active cardiac arrhythmias are generally divided into two major categories: (1) enhanced or abnormal impulse formation and (2) reentry. Reentry can be subdivided into three subcategories: (1) circus movement, (2) reflection, and (3) Phase 2 reentry. Reentry occurs when a propagating impulse fails to die out after normal activation of the heart and persists to re-excite the heart after expiration of the refractory period. Evidence implicating reentry as a mechanism of cardiac arrhythmias stems back to the turn of the century. Amplification of intrinsic electrical heterogeneities provides the substrate responsible for developing Phase 2 and circus movement reentry, which underlie ventricular tachycardia in the long QT and Brugada syndromes.

Animals↗
PubMed1979

Three social-preference measures in PKU monkeys.

Of twenty-four one-year-old rhesus, half were brain damaged from excessive phenylalanine (PKU) administered either pre- or post-natally. When compared on three measures of affiliation--(a) a simultaneous forced-choice proximity circus test, (b) a sequential free-operant Butler-box test, and (c) a social group in a playroom--the duration measure of the circus gave the best differentiation between stimulus animals, the Butler box the poorest. Both types of PKU monkeys were found to strongly prefer familiar PKU monkeys, and controls to refer unfamiliar followed by familiar controls. This extends preference research to induced brain damage and confirms behavioural abnormality in PKU macaques, an abnormality detectable by both humans and other monkeys.

Animals↗
PubMed1984

Irregular pacemaker tachycardia in a patient with WPW syndrome and an A-V universal pacemaker.

We describe a case of an irregular pacemaker circus movement tachycardia in a patient with the Wolff-Parkinson-White syndrome and a normally functioning A-V universal (DDD) pacemaker (Cordis Sequicor 233 D). The mechanism of the artificial circus movement tachycardia, which uses the pacemaker as the anterograde limb and a septally located accessory atrioventricular pathway as the retrograde limb, is discussed.

Atrioventricular Node↗
PubMed2004

Helicobacter acinonychis: genetic and rodent infection studies of a Helicobacter pylori-like gastric pathogen of cheetahs and other big cats.

Insights into bacterium-host interactions and genome evolution can emerge from comparisons among related species. Here we studied Helicobacter acinonychis (formerly H. acinonyx), a species closely related to the human gastric pathogen Helicobacter pylori. Two groups of strains were identified by randomly amplified polymorphic DNA fingerprinting and gene sequencing: one group from six cheetahs in a U.S. zoo and two lions in a European circus, and the other group from a tiger and a lion-tiger hybrid in the same circus. PCR and DNA sequencing showed that each strain lacked the cag pathogenicity island and contained a degenerate vacuolating cytotoxin (vacA) gene. Analyses of nine other genes (glmM, recA, hp519, glr, cysS, ppa, flaB, flaA, and atpA) revealed a approximately 2% base substitution difference, on average, between the two H. acinonychis groups and a approximately 8% difference between these genes and their homologs in H. pylori reference strains such as 26695. H. acinonychis derivatives that could chronically infect mice were selected and were found to be capable of persistent mixed infection with certain H. pylori strains. Several variants, due variously to recombination or new mutation, were found after 2 months of mixed infection. H. acinonychis ' modest genetic distance from H. pylori, its ability to infect mice, and its ability to coexist and recombine with certain H. pylori strains in vivo should be useful in studies of Helicobacter infection and virulence mechanisms and studies of genome evolution.

Acinonyx↗
PubMed1988

Reentrant and focal arrhythmias in low potassium in isolated rabbit atrium.

In isolated superfused left atria of the rabbit, tachyarrhythmias became highly inducible with a decrease of the extracellular potassium concentration to 2.0 mM. The nature of the arrhythmias was determined with a high-resolution mapping system. In several cases, abnormal impulse formation was found, but the majority of arrhythmias (75%) was caused by a circus movement of the impulse. Furthermore, circus-movement tachyarrhythmias often degenerated into fibrillatory activity, and activation maps revealed the presence of multiple wavelets during this chaotic rhythm. The occurrence of reentrant arrhythmias may be caused either by an increase in inhomogeneity in conduction or by a shortening of the wavelength in low potassium. Inhomogeneity in conduction was determined by calculating the difference in activation times between neighboring electrodes. In low potassium, premature activation significantly increased the inhomogeneity index compared with slow rhythm (from 2.2 to 3.9; P less than 0.001) but was not significantly different from the inhomogeneity measured at normal potassium concentrations. Low potassium, however, did shorten significantly the wavelength of the impulse by approximately 40%. The increased inducibility of reentry in low potassium is therefore caused by a reduction of the length of the excitation wave and not by an increase in inhomogeneity in conduction.

Animals↗
PubMed1983

Value of QRS alteration in determining the site of origin of narrow QRS supraventricular tachycardia.

To determine the value of alternation of QRS morphology in determining the site of origin of sustained narrow QRS supraventricular tachycardia (SVT), we retrospectively studied 163 distinct tachycardias in 161 patients (ages 4 to 91 years) in whom the site of origin of SVT was proven by intracardiac electrophysiologic study. Sustained SVT was defined as lasting longer than 30 sec. Narrow QRS was defined as QRS width less than 0.12 sec. Atrial fibrillation and flutter were excluded. The presence or absence of QRS alternation was judged at least 10 sec after initiation of SVT. Circus movement tachycardia with anterograde AV node conduction and a retrograde accessory AV pathway was seen in 89 patients (58 with Wolff-Parkinson-White syndrome, 31 with concealed accessory pathway); intra-AV nodal reentrant tachycardia (AVNT) was present in 57 cases, and 17 tachycardias were atrial in origin. QRS alternation was present in 36 of 163 cases (22%). In only eight of these 36 did RR interval length alternation accompany alternation in QRS morphology. Thirty-three of 36 (92%) tachycardias with QRS alternation were circus movement tachycardias. Two were atrial in origin and one was AVNT. We conclude that the presence of QRS alternation during sustained narrow QRS SVT is highly indicative of a retrograde accessory AV pathway in the tachycardia circuit.

Adolescent↗
PubMed1984

Intra-atrial reentry as a mechanism for atrial flutter induced by acetylcholine and rapid pacing in the dog.

In the isolated blood-perfused canine heart we produced episodes of rapid atrial flutter by continuous infusion of acetylcholine and rapid pacing. The spread of excitation during atrial flutter was mapped with the aid of two endocavitary mapping electrodes containing 960 leads and recording from 192 different sites simultaneously. The flutter maps clearly showed that intra-atrial reentry was the mechanism responsible for the arrhythmia. However, the localization and size of the intra-atrial circuits differed from case to case even in the same heart. The orifices of the venae cavae or the atrioventricular ring did not serve as a central anatomic obstacle for circus movement. We also failed to identify a special role of the internodal pathways in the formation of the loop. Instead, the intra-atrial circuits could be found everywhere, provided sufficient atrial mass was available to accommodate the circuit. The diameter of the circuits varied between 1.5 and 3 cm at a cycle length between 65 and 155 msec. The average conduction velocity of the circulating impulse varied between 60 and 80 cm/sec. Spontaneous termination of atrial flutter frequently occurred and was based on local conduction block in a narrow part of the circuit. Another interesting aspect of these studies is the finding that during continuous circus movement of the impulse, the amount of myocardium that is activated may vary considerably. This marked periodicity in excited tissue mass during atrial flutter could adequately explain the continuously undulating baseline or typical sawtoothlike F waves as seen in the surface electrocardiogram during atrial flutter.

Acetylcholine↗
PubMed1987

Effect of procainamide and N-acetylprocainamide on atrial flutter: studies in vivo and in vitro.

We studied the effects of procainamide and N-acetylprocainamide (NAPA) in a conscious dog preparation of atrial flutter resulting from circus movement around the tricuspid orifice. We also recorded transmembrane potentials of atrial tissues from the circus path in vitro. In 12 instrumented dogs, average flutter cycle length was 157 msec, the duration of the excitable gap was 73 msec, and conduction velocity was 0.75 m/sec. At 4 and 8 mg/kg, procainamide moderately prolonged cycle length, but did not terminate the flutter. At a cycle length of 300 msec procainamide increased effective refractory period (ERP) by 12% and 20% and conduction time by 8% and 19%. At 16 and 32 mg/kg procainamide prolonged cycle length, ERP, and conduction time by 60% to 80% and stopped the flutter in all trials. NAPA, at 16, 32, and 64 mg/kg, increased flutter cycle length by 16%, 16%, and 31%, ERP by 14%, 28%, and 41%, and conduction time by less than 15%. NAPA terminated the flutter in two of six dogs given 32 mg/kg, and three of five dogs given 64 mg/kg. The excitable gap was lengthened by both procainamide and NAPA. Transmembrane potentials showed that at a cycle length from 1000 to 300 msec procainamide (10 mg/liter) increased action potential duration and decreased the first time derivative of phase O of the action potential (Vmax), whereas NAPA (20 mg/liter) increased action potential duration without changing Vmax. These findings show the difficulty of relating drug effects on transmembrane potentials to efficacy in vivo since the former do not necessarily indicate which changes in cellular electrical activity are responsible for efficacy against a particular arrhythmogenic mechanism.

Acecainide↗
PubMed1991

Anatomy of the tricuspid annulus. Circumferential myofibers as the structural basis for atrial flutter in a canine model.

BACKGROUND: Little anatomic information is available on the annular myocardium. This study was conducted to determine the anatomic substrate for atrial flutter due to circus movement around the tricuspid annulus in the Y-shaped incision canine model of atrial flutter. METHODS AND RESULTS: We studied photographs of the annular myocardium serial histological sections, made in either of three different planes, and compared these with photographs of the intact and blocked gross heart specimens. We found that the annulus is the most caudal region of the atrial wall. The epicardial aspect of the annulus abuts the ventricular septum or the aortic root in the medial region; in other regions, it is covered by the fat of the coronary sulcus. Its endocardial aspect is delimited by the tricuspid leaflets inferiorly and by the pectinate muscle bundles superiorly, except in the medial region where the pectinate muscle bundles are absent. The annular myocardium is bilaminated. A continuous subepicardial circumferential lamina is the most prominent and is robust in the anterior, lateral, and posterior regions, but it attenuates to a fine muscular connection in the medial region. Myofibers of its superior border merge with the pectinate muscle bundles or are admixed in the medial region with myocardium at the base of the medial atrial wall. Its inferior border makes little contact with the annulus fibrosus about the ring; however, in the medial region, these myofibers insert into fibrous tissue superior to the septal leaflet. A discontinuous, subendocardial perpendicular lamina contains myofibers that descend from the atrium; most of these myofibers insert into the annulus fibrosus about the ring, but the lamina is absent in the anteromedial region. CONCLUSIONS: We conclude that the continuous circumferential lamina provides the anatomic substrate for circus movement of excitation in this model.

Animals↗
PubMed1977

Action potentials, afterpotentials, and arrhythmias.

Triggered activity must be added to spontaneous activity and to circus movement as a cause for extrasystoles and tachycardias of either atrial or ventricular origin. The activity of a triggerable focus requires phase 4 depolarization caused by an afterpotential; this distinguishes it from the activity seen in circus movement. A triggerable focus becomes rhythmically active only if driven at a critical rate or by a critically timed premature impulse; this distinguishes it from a focus of spontaneous or automatic activity. The ease of triggering a triggerable focus increases in the presence of catecholamines; triggerable foci in the atrium become quiescent when exposed to acetylcholine. At the present time, fibers within the coronary sinus provide the most persuasive example of triggered activity as a possible cause of arrhythmias of clinical significance. It is possible that the coupled extrasystoles of digitalis toxicity may be triggered; there is every reason to believe that further examples of triggered arrhythmias of possible clinical significance will be discovered.

Action Potentials↗
PubMed1989

Mechanisms of termination of reentrant atrial arrhythmias by class I and class III antiarrhythmic agents.

We studied atrial flutter due to circus movement in chronically instrumented conscious dogs to identify the mechanism by which class I and class III antiarrhythmic drugs terminate reentrant excitation. We used a crossover experimental design administering five class I agents and one class III agent, by intravenous bolus followed by intravenous infusion. The class I agents other than lidocaine were almost uniformly effective in terminating the arrhythmia (disopyramide in six of seven dogs, propafenone in six of six, flecainide in seven of seven, and SC-40230 in seven of seven). Termination was preceded by a marked increase in cycle length (ranging from +78% with propafenone to +55% with disopyramide), but with the exception of disopyramide, class I agents did not significantly shorten the excitable gap. With disopyramide the gap decreased from 49 +/- 3% to 28 +/- 3% of the cycle length. With no class I agent did the wavelength of effective refractoriness increase to approach the cycle length of the arrhythmia. Lidocaine, used as a negative control, terminated the reentry in one dog with modest prolongation of the cycle length. Terminations with class I agents correlated with depression of conduction rather than prolongation of refractoriness. In contrast with class I agents, D-sotalol prolonged the cycle length minimally (+10%) and terminated the arrhythmia in six of seven dogs. It decreased the excitable gap from 42 +/- 4% to 26 +/- 6% of the cycle, but it still did not cause the wavelength of effective refractoriness to equal the cycle length. Terminations by D-sotalol seemed to result from either failure of the lateral boundaries of the circus path or reflection within the path.

Animals↗
PubMed1989

Stimulus-induced critical point. Mechanism for electrical initiation of reentry in normal canine myocardium.

The hypothesis was tested that the field of a premature (S2) stimulus, interacting with relatively refractory tissue, can create unidirectional block and reentry in the absence of nonuniform dispersion of recovery. Simultaneous recordings from a small region of normal right ventricular (RV) myocardium were made from 117 to 120 transmural or epicardial electrodes in 14 dogs. S1 pacing from a row of electrodes on one side of the mapped area generated parallel activation isochrones followed by uniform parallel isorecovery lines. Cathodal S2 shocks of 25 to 250 V lasting 3 ms were delivered from a mesh electrode along one side of the mapped area to scan the recovery period, creating isogradient electric field lines perpendicular to the isorecovery lines. Circus reentry was created following S2 stimulation; initial conduction was distant from the S2 site and spread towards more refractory tissue. Reentry was clockwise for right S1 (near the septum) with top S2 (near the pulmonary valve) and for left S1 with bottom S2; and counterclockwise for right S1 with bottom S2 and left S1 with top S2. The center of the reentrant circuit for all S2 voltages and coupling intervals occurred at potential gradients of 5.1 +/- 0.6 V/cm (mean +/- standard deviation) and at preshock intervals 1 +/- 3 ms longer than refractory periods determined locally for a 2 mA stimulus. Thus, when S2 field strengths and tissue refractoriness are uniformally dispersed at an angle to each other, circus reentry occurs around a "critical point" where an S2 field of approximately 5 V/cm intersects tissue approximately at the end of its refractory period.

Animals↗
PubMed2002

From Elephant Man to Jerry Springer: the rise of the psychological tele-spectacle.

In the circus sideshow, people with physical deformities were exhibited for profit and entertainment. The circus sideshow itself is no longer socially acceptable, but it has taken a different form. Television programs like The Jerry Springer Show make spectacles of psychological afflictions and variations in human behavior. On the one hand, these shows provide participants with attention, recognition, an outlet for masochism, and an identity. To the viewer, they offer both reassurance and an outlet for unacceptable thoughts and feelings. They also explore society's collective subconscious. On the other hand, these shows approximate psychological interventions without concern for the result, have potentially negative consequences for vulnerable viewers, and blur the boundary between fantasy and real life.

Journal Article↗