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PubMed1984

Clinical efficacy and electrophysiologic effects of intravenous and oral encainide in patients with accessory atrioventricular pathways and supraventricular arrhythmias.

The electrophysiologic effects and clinical efficacy of intravenous (i.v.) and oral encainide were studied in 13 patients with accessory atrioventricular (AV) pathways (7 overt, 1 intermittent and 5 concealed) and drug-resistant supraventricular arrhythmias (5 paroxysmal atrial fibrillation, 1 atrial tachycardia and 7 with orthodromic circus movement tachycardia). Previously, therapy had failed with a mean of 3 conventional antiarrhythmic agents. In 5 patients, amiodarone administration had also been unsuccessful. All patients underwent programmed electrical stimulation of the heart before and after 1.5 mg/kg of i.v. encainide. Seven patients were restudied during oral encainide therapy (mean 155.8 +/- 54.2 mg/day) 3 days to 6 weeks (average 21 days) later. Anterograde conduction over the accessory AV pathway blocked in 4 of 7 patients after i.v. encainide. Oral encainide blocked anterograde conduction over the accessory pathway or prolonged the refractory period of the accessory pathway in 3 of 4 patients. This change in anterograde conduction was independent of the predrug value for the anterograde refractory period of the accessory AV pathway. Intravenous and oral encainide had minimal effects on retrograde conduction over the accessory AV pathway. The clinical effect of oral encainide was studied in 12 patients. Four patients responded to oral encainide and have been free of arrhythmia or side effects for 2 to 20 months (average 10.5). Encainide failed to prevent the clinical arrhythmia in 2 patients. In 4 patients with atrial arrhythmias, circus movement tachycardia developed during oral encainide therapy. In 1 patient the frequency of circus movement tachycardia increased with oral encainide treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

The electrocardiogram in patients with multiple accessory atrioventricular pathways.

The 12 lead electrocardiographic (ECG) findings were reviewed in 17 patients having two or more accessory pathways as documented during electrophysiologic study in all 17 patients and by intraoperative mapping in 8. Twelve patients had findings suggesting the presence of more than one atrioventricular (AV) pathway. These were 1) more than one P wave configuration during orthodromic circus movement tachycardia (four patients); 2) a "mismatch" between the location of the ventricular and atrial ends of the accessory pathway as assessed when comparing exclusive AV and ventriculoatrial conduction over the accessory pathway during antidromic and orthodromic circus movement tachycardia, respectively (seven patients); 3) atrial fibrillation showing more than one pre-excitation pattern (six patients); 4) a spontaneous change from orthodromic to antidromic circus movement tachycardia and vice versa (two patients); 5) a spontaneous change from one type of antidromic tachycardia to another (two patients); and 6) a change in pre-excitation pattern after administration of a drug that prolongs the anterograde refractory period of the accessory pathway (three patients). The retrospective nature of this study does not allow conclusions as to the true value of the ECG in predicting the presence of more than one accessory pathway. This issue needs to be evaluated in a prospective study.

Adolescent↗
PubMed1989

Monophasic action potentials during reentrant atrial flutter in the dog: effects of clofilium and acetylcholine.

Monophasic action potentials (MAP) were recorded from canine atrium during reentrant flutter resulting from circus movement in atrial tissue above the tricuspid ring. A catheter and plaque contact electrodes were developed to record MAP from the epicardium or endocardium during sinus rhythm, paced rhythms, and flutter. The transmembrane action potential duration of tricuspid ring tissue also was studied in vitro. During flutter at cycle lengths of 140-160 ms, MAP showed incomplete repolarization. Pacing at comparable cycle lengths had a similar effect. Acetylcholine (10 micrograms/kg, i.v.) shortened MAP duration during pacing and, during flutter, decreased cycle length and increased MAP amplitude. Clofilium (500 micrograms/kg, i.v.) prolonged flutter cycle length by 18% and terminated the flutter within 30-120 s. During pacing at a cycle length of 300 ms, clofilium increased MAP duration and effective refractory period (ERP) by 30%. Transmembrane action potentials showed that clofilium (0.2 mg/L) modified only action potential duration. Conduction velocity was significantly decreased by clofilium during flutter but not during pacing at a cycle length of 300 ms. These data support the conclusion that in this model of flutter, the circus movement occurs in partially repolarized tissue. The circus movement can be accelerated by agents (acetylcholine) that reduce ADP, and slowed and terminated by agents (clofilium) that increase it.

Acetylcholine↗
PubMed1991

Transitions among atrial fibrillation, atrial flutter, and sinus rhythm during procainamide infusion and vagal stimulation in dogs with sterile pericarditis.

The mechanism of atrial flutter and fibrillation induced by rapid pacing in 22 dogs with 3-day-old sterile pericarditis was investigated by computerized epicardial mapping of atrial activation before and after administration of agents known to modify atrial electrophysiologic properties: procainamide, isoproterenol, and electrical stimulation of the vagosympathetic trunks. Before the administration of any of these agents, a total of 30 episodes of sustained atrial flutter (greater than 1 min duration, monomorphic; regular cycle length, 127 +/- 12 ms, mean +/- SD) was induced in 15 out of 22 dogs and 9 episodes of unstable atrial flutter (duration, less than 1 min; cycle length, 129 +/- 34 ms; monomorphic, alternating with fibrillation) were induced in the remaining 7 preparations. In the latter, administration of procainamide transformed unstable atrial flutter and atrial fibrillation to sustained atrial flutter (cycle length, 142 +/- 33 ms; n = 9 episodes). During control atrial flutter, atrial maps displayed circus movement of excitation in the right atrial free wall with faster conduction parallel to the orientation of intra-atrial myocardial bundles. Vagal stimulation changed atrial flutter to atrial fibrillation in 32 of 73 trials; this was associated with acceleration of conduction in the lower right atrium, leading to fragmentation of the major wave front. Isoproterenol produced a 6-25% increase of the atrial rate in 6 out of 14 trials of atrial flutter and induced atrial fibrillation in 4. After procainamide, the reentrant pathway was lengthened and conduction was slowed further in the right atrium. Maps obtained during unstable atrial flutter showed incomplete circuits involving the right atrium. Following procainamide infusion, the area of functional dissociation or block was enlarged and a stable circus movement pattern, which was similar to the pattern seen in control atrial flutter, was established in the right atrium. We conclude that (1) the transitions among atrial fibrillation, atrial flutter, and sinus rhythm occur between different functional states of the same circus movement substratum primarily located in the lower right atrial free wall, and (2) the anisotropic conduction properties of the right atrium may contribute to these reentrant arrhythmias and may be potentiated by acute pericarditis.

Animals↗
PubMed1984

Mapping of ventricular tachycardia induced by programmed stimulation in canine preparations of myocardial infarction.

To investigate the mechanism of uniform ventricular tachycardia induced by programmed stimulation, we recorded His bundle electrograms and unipolar electrograms from 64 subepicardial, subendocardial, and intramural sites in dogs. Isochronal maps were generated off-line by computer. Two groups of dogs were studied 3 days after occlusion of their left anterior descending coronary arteries; one group underwent reperfusion after 2 to 2.5 hr of occlusion and the other methylprednisolone treatment before permanent occlusion. In the former, subepicardial sequences presented either a pattern suggesting circus movement or a radial pattern in which excitation at intramural sites could precede earliest subepicardial excitation. In the latter preparations, subepicardial excitation patterns consistently suggested circus movement in the subepicardial muscle layer surviving over necrotic tissue. Assuming complete circus movement, the "missed" time interval, measured as the interval left unaccounted for by actual recording of local excitation between ventricular tachycardia cycles, ranged from 3% to 64% of the cycle length of ventricular tachycardia. While surviving subepicardial and intramural layers appeared to be involved in the mechanism of ventricular tachycardia, a late second breakthrough on the right ventricle, in conjunction with fixed-coupled H deflections on the His bundle electrograms, suggested the involvement of the conducting system in propagation of the impulse.

Animals↗
PubMed1980

Computer simulation of arrhythmias in a network of coupled excitable elements.

Arrhythmias were simulated in sheets or cables, consisting of coupled excitable elements, which were characterized by a simple regenerative mechanism. The geometry of the network, the amount of coupling among individual elements, and the properties of the elements relating to excitability, automaticity, and duration of the refractory period could be adjusted arbitrarily in an interactive computer program. When a critical amount of coupling was present between automatic and non-automatic cells, sustained repetitive activity could be initiated and stopped by stimulation of the elements. Using this mechanism, it also was possible to evoke reciprocal activity in a one-dimensional cable. In uniform sheets of coupled elements, circus movement of the activation front could be evoked. The presence of an obstacle or dispersion of the refractory periods of the elements was not a prerequisite for the initiation of circus movements. The vortex of circus movements in the homogeneous sheets consisted of elements which were inactivated by depolarizing currents from the circulating wavefront. In sheets of sufficient size, multiple vortices could be present.

Action Potentials↗
PubMed1986

Atrial reentry around an anatomic barrier with a partially refractory excitable gap. A canine model of atrial flutter.

We have characterized, in dogs, a model of inducible regular atrial tachycardia that resembles atrial flutter. The model involves creating a Y-shaped lesion comprised of an intercaval incision and a connected incision across the right atrium. It is suitable for serial studies of the effects of pacing or antiarrhythmic drugs in chronically instrumented animals studied in the awake state for at least several months. The postoperative cycle length of the induced tachycardia varies from 143 to 188 msec, depending on the size of the dog. The tachycardia cycle length was consistent for each dog, and the rhythm--once induced--was very stable until terminated by pacing. The mechanism of the tachycardia was reentry due to circus movement based on the ability to induce and terminate it by premature impulses or overdrive, the ability to reset the tachycardia by single premature stimuli, the pattern of entrainment during overdrive stimulation, and the ability to terminate the tachycardia by interrupting the conduction pathway. The window of reset determined by the range of coupling intervals of premature stimuli that were able to enter and reset the tachycardia ranged from 56 to 82 msec. There appears to be incomplete recovery of excitability by the end of the excitable gap as evidenced by the fact that even late premature impulses that enter the reentrant circuit conduct more slowly than the tachycardia impulse, and because stimulation of muscarinic receptors that shortens the duration of the action potential and refractoriness also reduces the cycle length of the tachycardia. Epicardial and endocardial activation mapping during tachycardia showed the reentrant pathway does not merely encircle the lesion, particularly over the left atrial epicardium near the intercaval lesion. Rather, the impulse appears to travel around the atrial tissue just above the tricuspid ring, including a portion that travels through the right side of the lower intraatrial septum. Thus, the model involves circus movement around an anatomic barrier through normal tissue that contains no depressed segments. During the circus movement, there is a relatively long excitable gap during which there is incomplete recovery of excitability. This model should be useful for studies of the mechanism of antiarrhythmic drug action and the responses to premature stimulation in this particular subclass of reentrant rhythms, and for comparison with the behavior and responses of other forms of reentry.

Animals↗
PubMed1975

The mechanism of supraventricular tachycardia induced by a single premature beat in the isolated left atrium of the rabbit. II. The termination of the tachycardia.

Tachycardias induced by a single stimulus in the left atrium of the rabbit, are based on a circus movement of the impulse through the atrial myocardium. Circus movement often stopped spontaneously after only one beat ("coupled extrasystole") or after a small number of beats. This frequent early cessation of circus movement is explained by the relatively high conduction velocity and relatively long refractory period in the early stage of tachycardia. As an exception tachycardia lasted for a longer period. The circulating impulse then could always be interrupted by the application of a properly timed stimulus. In this case the circulating impulse will encounter the activation wave elicited by the stimulus. This resulted either in termination or resetting of the tachycardia.

Action Potentials↗
PubMed1976

Pathophysiological basis of tachyarrhythmias--re-entry.

A description is given of the principles of re-entry and circus movement, which were originally formulated on the basis of experiments on jellyfish and play an important role in cardiac arrhythmias. The essential features of re-entry are 1) the existence of two conducting pathways which communicate at their proximal and distal ends, and 2) the occurrence of uni-directional block in one pathway while conduction is maintained in the other. A retrograde wavefront may then be set up in the pathway where block was present, and the tissue from which the impulse came may be re-excited. Once this sequence is set up it may continue as a circus movement leading to tachycardia. Long re-entry circuits are present in Wolff-Parkinson-White syndrome, in which two connections between atria and ventricles exist. Micro-re-entry may occur in a variety of cardiac tissues. An example of supraventricular tachycardia due to micro-re-entry in the atrio-ventricular node of an isolated rabbit heart is shown, in which simultaneous recording of transmembrane potentials of AV nodal cells unraveled the events. The principles of the termination of circus movement tachycardias by electrically induced premature beats are discussed.

Atrioventricular Node↗
PubMed1994

Radiofrequency catheter ablation of both atrial ventricular nodal reentrant and atrial ventricular reentrant tachycardia in a single session.

Radiofrequency catheter ablation is a new therapeutic approach to treat patients with symptomatic drug-resistant paroxysmal supraventricular tachycardia. Ablation of two accessory atrioventricular pathways in a single session has been frequently described previously. However, ablation in a single session of both the fast pathway, involved in atrial ventricular nodal reentrant tachycardia, and a concealed atrioventricular accessory pathway involved in a circus movement tachycardia has rarely been reported. A 57-year-old man with a grade III aortic incompetence had the infrequent association of atrial ventricular nodal reentrant tachycardia and orthodromic circus movement tachycardia due to a concealed accessory pathway. He presented with drug-resistant reentrant supraventricular tachycardia and, in a single session, underwent a successful radiofrequency catheter ablation of the fast atrial ventricular nodal pathway and a concealed posteroseptal accessory pathway. During a 10-month follow-up he was free of palpitations without any antiarrhythmic therapy and underwent elective aortic valve replacement.

Catheter Ablation↗
PubMed1975

Genesis of arrhythmias and mechanism of electrical defibrillation of the heart.

Atrial arrhythmias were induced in experiments on dogs by electrical stimulation or by local application of aconitine and methacholine to the atrium. The action of the defibrillator discharge on these arrhythmias was studied. The defibrillator discharge abolished the arrhythmias maintained by the circus movement of the excitation wave over the atria but did not abolish sinus tachycardia or ectopic aconitine tachysystoles. The threshold of the defibrillating effect depends on the existence of micro-or macro-reentries. Thmechanism of defibrillation consists of excitation of the atrial myocardium with a consequent decrease in the pathway for the circulation of excitation to below the critical size for maintaining the circus movement of the excitation wave. The axtion of the defibrillator does not inihibit the automatism of the nomotopic and heterotopic cardiac pacemakers.

Aconitum↗
PubMed1987

Reflections on reentry and focal activity.

Initiation and maintenance of reentrant arrhythmias, such as ventricular tachycardia and fibrillation in the acute phase of myocardial ischemia, may be due to different mechanisms. The characteristics of circus movement reentry, both with and without involvement of an anatomic obstacle, are discussed. The concept of wavelength of a reentrant circuit as calculated by the product of refractory period and conduction velocity is emphasized. To maintain circus movement tachycardia in an acutely ischemic myocardium, the ischemic tissue mass must be larger than the wavelength. For maintenance of fibrillation, several independent reentrant wavelets must be simultaneously present. Agents that prolong wavelength (by lengthening refractory period, increasing conduction velocity or both) may prevent reentry. Experiments are described that show the effectiveness of lidocaine, which depresses action potentials of ischemic myocardial cells, in preventing ventricular fibrillation when administered before coronary artery occlusion in isolated pig hearts. Ventricular premature depolarizations or beats are usually necessary to initiate reentrant rhythms. They may be caused by reflection, a type of reentrant excitation involving slow conduction, or by electronic transmission over short segments of depressed or unexcitable tissue. An example of microreentry in a 4 mm segment of papillary muscle exposed to elevated extracellular K+ concentrations, resulting in a ventricular premature beat, is shown. Focal mechanisms, such as abnormal automaticity or triggered activity, may also be responsible for premature impulses. Agents that suppress premature depolarizations may be effective against reentrant arrhythmias, even when they do not affect the reentrant mechanism itself. Experiments are described, showing that moricizine HCl suppresses abnormal automaticity in isolated papillary muscle, partially depolarized by application of electric current.

Animals↗
PubMed1988

Characteristics of entrainment during autodecremental atrial and ventricular stimulation.

The entrainment characteristics of orthodromic circus movement tachycardias occurring during autodecremental atrial and ventricular stimulation were studied in 9 patients with manifest Wolff-Parkinson-White syndrome. The phenomenon occurred in 34 of 38 episodes of tachycardia during autodecremental atrial stimulation. It was not seen in 4 episodes because the first impulse penetrating the circuit terminated the arrhythmia. Invariably, the HH and VV intervals were not equal to, but longer than, the stimulus-stimulus intervals, thus not fulfilling the definition of "classic" (constant cycle length) entrainment postulated by Okumura et al. Furthermore, the first 2 of the 3 diagnostic criteria were not demonstrated and the third only could be demonstrated in 7 episodes. Tachycardia termination was achieved in all 38 episodes. Entrainment occurred during autodecremental ventricular stimulation in 79 of 80 episodes, with the AA and H-H- intervals (when visible) being equal to the corresponding paced cycle lengths. Moreover, the intervals between the last paced ventricular beat and the first ventricular beat of the resumed tachycardia were invariably longer than the last stimulus-stimulus intervals. These characteristics were those which Okumura et al attributed to "concealed" entrainment. Tachycardia termination was achieved in 77 of 80 episodes. In summary: (1) autodecremental atrial pacing produced a specific form of entrainment that did not fulfill the "classic" definition of Okumura et al; (2) autodecremental ventricular pacing consistently produced "concealed" entrainment; and (3) autodecremental stimulation was very effective in terminating 115 of 118 (98%) of episodes of circus movement tachycardias.

Cardiac Pacing, Artificial↗
PubMed1989

Intravenous diltiazem in patients with paroxysmal re-entrant supraventricular tachycardia.

The electrophysiologic effects and efficacy of diltiazem were evaluated with programmed electrical stimulation of the heart in 12 patients with supraventricular re-entrant tachycardia (five with atrioventricular nodal tachycardia and seven with circus movement tachycardia the accessory pathway being concealed in 4). Diltiazem was infused over 1 minute at the dose of 0.25 mg/kg and the electrophysiologic parameters were evaluated at 5 and 30 minutes. Diltiazem prolonged the AH interval from 83.5 +/- 58 to 99 +/- 55 msec (P less than 0.05), effective and functional refractory periods of atrioventricular node from 244 +/- 40 to 268 +/- 56 msec (P less than 0.05) and from 432 +/- 124 to 468 +/- 130 msec (P less than 0.005) respectively, lowered the atrial pacing rate inducing second-degree atrioventricular block from 159 +/- 32 to 134 +/- 33 beats/min (P less than 0.005) and decreased systolic and diastolic blood pressure from 143.5 +/- 33 to 132.5 +/- 22 mm Hg (P less than 0.05) and from 90 +/- 15 to 82.5 +/- 9 (P less than 0.05), respectively. Diltiazem prevented the reinduction of the tachycardia in 4 of 5 patients with atrioventricular nodal tachycardia and in 4 of 7 with circus movement tachycardia. The mechanism of action of diltiazem consisted of depression of conduction in atrioventricular node in anterograde fashion while there were no effects on refractoriness of the accessory pathway. The drug was well tolerated with no adverse effects. Diltiazem, therefore, appears an effective and safe drug in the acute treatment of re-entrant supraventricular tachycardia.

Adolescent↗
PubMed2005

Septicaemia secondary to infection by Corynebacterium macginleyi in an Indian python (Python molurus).

A seven-year-old female Indian python (Python molurus) weighing about 35kg was euthanased after several clinical episodes of stomatitis, pneumonia, ophthalmitis and dystocia over a period of four years. The animal had been maintained in a terrarium in a circus truck at an adequate temperature. During shows, however, the snake was considered to be exposed to stressful conditions for several hours at a time at low temperatures and with noise and bright lights. A post-mortem examination indicated ulcerative stomatitis, osteomyelitis, severe pneumonia and numerous granulomata and multifocal necrosis in stomach and spleen. Corynebacterium macginleyi was isolated in pure culture from the ulcerative stomatitis, and mixed with Stenotrophomonas maltophilia from the lungs and spleen. The findings indicated that the snake had died from a septicaemic process caused by C. macginleyi, probably originating from the stomatitis. The role of S. maltophilia as a secondary agent is discussed. The stress of the circus show and poor husbandry may have predisposed the animal to infection and septicaemia. This is the first report of C. macginleyi causing disease in a snake.

Animals↗
PubMed1975

Junctional reciprocating tachycardias. The permanent and paroxysmal forms of A-V nodal reciprocating tachycardias.

Stimulation technics have demonstrated a reciprocating mechanism in many supraventricular tachycardias previously classified from a purely morphologic point of view. Three conditions are required for the creation of a circus movement: a potential circuit pathway, undirectional block in this curcuit, and slowed conduction. While all three conditions are readily apparent in reciprocating tachycardias of the WPW syndrome, two or even all of these factors may be concealed in the others forms. Paroxysmal reciprocating tachycardias are characterized by prolongation of the P-R interval in the beat immediately preceding the tachycardia, and are generally accepted as being related to longitudinal dissociation of the A-V node, though the possibility of unidirectional (anterograde) block of an extra-nodal accessory pathway should be appreciated. Permanent reciprocating tachycardias start after a normal P-R interval when the sinus cycle reaches a critical value. Both paroxysmal and permanent forms of reciprocating tachycardia must be differentiated from tachycardias located in the atria: one of the most reliable features of reciprocating tachycardia is the existence of a 1:1 A-V relationship which cannot be altered without interrupting the tachycardia. Study of capture phenomena during the tachycardia, and the modes of termination not only permit the demonstration of the reentry mechanism but may also determine more precisely the actual location of the circus movement.

Adult↗
PubMed1992

Studies on re-entrant arrhythmias and ectopic beats in excitable tissues by bifurcation analyses.

A phase-plane bifurcation analysis is a useful way to theoretically understand how various types of arrhythmias may arise from excitable tissues. In this paper, we have performed phase-plane bifurcation analysis to characterize arrhythmogenic states in excitable tissues. To achieve this, we have first formulated a model which is simple enough to be mathematically tractable, yet captures the non-linear features of cardiac excitation and conduction. In this model, single cells are connected in a circular fashion by gap conductances. Each cell carries the following two types of currents: a passive outward current and an inward "excitable" current which contains an activation and an inactivation gate. The activation gate is responsible for the upstroke of action potential and inactivation gate is responsible for the termination of the plateau potential. With this model, we have constructed bifurcation diagrams as a function of a bifurcation parameter. The parameter chosen as the bifurcation parameter has the property of raising maximum diastolic potential while shorting the refractory period. Our analysis revealed the existence of three distinct multi-stable phases in certain ranges of the bifurcation parameter: (1) bistability between a rotor and a quiescent state, (2) bistability between rotor and ectopic beats, and (3) three stable states co-existing among quiescent state, rotor, and ectopic beats. In these three regions, external impulses exert very distinct effects: In region 1, a brief current pulse can annihilate a re-entrant arrhythmia to quiescence. To initiate re-entry from a quiescent tissue, however, it takes two pulses (a primary pulse followed by a premature pulse at a site different from the "primary" site). In region 2, a brief pulse can convert a re-entrant arrhythmia to ectopic beats. To convert the ectopic beats back to circus movement, these beats have to be suppressed by a few brief current pulses to initiate one-way propagation. Depending on the frequency and strength of impulses in region 3, the tissue can switch back and forth among quiescence, circus movement, and ectopic beats. For comparison, we have also included a more complete Beeler-Reuter cardiac cell model in our analysis and obtained essentially the same results. From the behavioral similarities of these models, we conclude that re-entrant and ectopic arrhythmias must be intrinsic properties of excitable tissues and external stimuli can convert one mode of arrhythmia to another in the multistability regions.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1996

Left-sided atrial flutter: characterization of a novel complication of pediatric lung transplantation in an acute canine model.

BACKGROUND: Postoperative atrial flutter has been observed in approximately 10% of children undergoing lung transplantation at our institution. We hypothesized that the left atrial anastomoses made to establish pulmonary venous continuity provide the primary electrophysiologic substrates for atrial flutter. OBJECTIVES: Our objectives were (1) to determine whether the left atrial suture lines alone are sufficient to produce atrial flutter in an acute canine model of lung transplantation and (2) to characterize any resulting reentrant circuits to surgically ablate the atrial flutter. METHODS: Supported by cardiopulmonary bypass, adult dogs (n = 10) underwent bilateral pneumonectomies. The left atrial anastomotic suture lines were simulated by dividing the tissue between the ostia of the transected superior and inferior pulmonary veins and closing the resulting defects. Bilateral suture lines were placed in group 1 (n = 6) to simulate bilateral lung transplantation. In group 2 (n = 4), only a left-sided suture line was placed to represent single lung transplantation. Unipolar 253-point biatrial endocardial mapping electrodes were inserted via bilateral ventriculotomies. Atrial flutter was induced by atrial burst pacing, and activation sequence maps were generated. In five of six cases in group 1, a T-incision connecting the two suture lines and the mitral anulus was then made. In group 2, a single incision from the suture line to the mitral anulus was performed in each case. Burst pacing was subsequently repeated. RESULTS: Atrial flutter could not be induced after bypass alone in any case. After simulated lung transplantation, sustained atrial flutter was reproducibly induced in 10 of 10 dogs. The mean cycle length in all dogs was 133 +/- 7 msec. There was no significant difference in mean cycle length or activation sequence patterns between groups 1 and 2. The reentrant circuit was confined to the left atrium. Each simulated left atrial anastomosis created a zone of conduction block around which circus movement could occur. In group 1, either suture line functioned as the central obstacle. Atrial flutter was terminated in five of five dogs in group 1 by means of the T-incision and in all four dogs in group 2 with the incision connecting the suture line to the mitral anulus. CONCLUSIONS: (1) In an acute canine model of lung transplantation, each left atrial suture line alone provides an electrophysiologic substrate for atrial flutter by creating a zone of conduction block around which circus movement can occur. (2) Extending this zone of block to the mitral anulus, together with interruption of the isthmus of tissue between the two suture lines present after bilateral lung transplantation, terminates the atrial flutter in this model and may have an application prophylactically at the time of lung transplantation in children to prevent postoperative atrial flutter.

Anastomosis, Surgical↗