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At least 19 recordsLinked to original sources
PubMed1992

Comparison of atrial overdrive pacing with and without extrastimuli for termination of atrial flutter.

Atrial overdrive pacing has been successfully used to terminate atrial flutter. This study compared the efficacy of atrial extrastimuli following a rapid pacing train to overdrive pacing without atrial extrastimuli for the termination of atrial flutter. Patients were randomized to treatments of short or long burst atrial overdrive pacing or atrial overdrive pacing followed by atrial extrastimuli in a crossover study design. A total of 22 patients (73%) had successful conversion of atrial flutter to sinus rhythm. The success rates in patients exposed to each therapy, including crossover therapies, were 62% with the atrial extrastimuli method, 8% with the short burst pacing method, and 8% with the long burst pacing method (p less than 0.001). Transient atrial fibrillation developed in 15 patients and in 9 of these this arrhythmia preceded conversion to sinus rhythm. Sustained atrial fibrillation was induced in 3 additional patients but never with the atrial extrastimuli method. In conclusion, the method of delivering atrial extrastimuli after a rapid pacing train is highly efficacious for the termination of atrial flutter. Furthermore, this method is more effective than atrial overdrive pacing methods delivered at the same pacing cycle length. These observations have important implications for the programming of antitachycardia pacemakers.

Aged↗
PubMed1977

Entrainment and interruption of atrial flutter with atrial pacing: studies in man following open heart surgery.

To examine the question of why the pacing rate and duration of atrial pacing are crucial factors in the successful interruption of atrial flutter, studies were performed on 30 patients in the period following open heart surgery. In each patient the diagnosis of atrial flutter was made using a pair of wire electrodes placed on the right atrial epicardium at the time of operation and brought out through the anterior chest wall. The same electrodes were used for atrial pacing. Pacing faster than the spontaneous rate of the atrial flutter which failed to interrupt the atrial flutter was associated with transient entrainment of the atrial flutter up to the atrial pacing rate. Atrial flutter was interrupted successfully when the atria were paced at a rate which was too fast for the atrial flutter to follow. This was heralded by the conversion of previously negative flutter waves to positive atrial complexes in ECG lead II. When pacing the atria at a constant rate, 2-22 seconds with a mean of 10 seconds were required to interrupt the atrial flutter.

Adult↗
PubMed1975

Termination of atrial flutter and atrial tachycardia with rapid atrial stimulation.

The results in this series of fifty-seven patients confirms the safety and reliability of rapid atrial stimulation to terminate atrial flutter and atrial tachycardia. Transthoracic wires implanted at thoracotomy or transvenously placed atrial electrodes can be used for the confident intracardiac electrocardiographic diagnosis of tachyarrhythmias and for atrial stimulation. Our experience represents the second largest reported series of patients to undergo cardioversion by this method. In all but five of fifty-seven patients either the atrial tachyarrhythmia was converted to normal sinus rhythm or the flutter-tachycardia was terminated with resultant atrial fibrillation. In forty-three patients sinus rhythm was eventually re-established after atrial stimulation. Various aspects of rapid atrial stimulation, including it's preference over precordial shock, have been discussed. We feel particular consideration should be given cardioversion by rapid atrial stimulation in patients with possible digitalis toxicity and in all patients who have atrial flutter, atrial tachycardia, or junctional tachycardia after open heart surgery.

Aged↗
PubMed1988

Shift of atrial reentrant tachycardia with transient entrainment to an uncommon and a common type of atrial flutter.

Atrial reentrant tachycardia (ART) which demonstrated transient entrainment shifted to an uncommon type of atrial flutter (AF) with premature atrial stimulation, and then returned to ART spontaneously. Subsequently, this ART shifted to a common type of AF by rapid atrial pacing, which was further transformed into an uncommon type of AF and finally terminated by rapid atrial pacing. The mechanism of AF in clinical cases is still controversial, but in this case, AF, both uncommon and common types, is considered due to macro-reentry within the atria. To explain the shift of ART to AF and mutual transformation between common and uncommon type of AF, we made a schematic figure of reentry loop within the atria of ART and AF.

Aged↗
PubMed1975

Atrial activity during exercise in patients with atrial flutter or atrial fibrillation.

The atrial activity was studied at rest and during exercise in 6 patients with atrial flutter and in 7 patients with atrial fibrillation. In the latter, a special recording technique was used which permitted identification of the f-waves. No increase in the frequency of the atrial waves was found. Thus the increase of the ventricular rate during work in patients with atrial flutter or atrial fibrillation seems to be caused by a change in the atrio-ventricular conduction.

Adult↗
PubMed1987

Effects of N-acetylprocainamide on experimental atrial flutter and atrial electrophysiologic properties in conscious dogs with sterile pericarditis: comparison with the effects of quinidine.

N-acetylprocainamide (NAPA) is said to have class III antiarrhythmic drug properties. The effects of NAPA (25 mg/kg intravenously) on sustained, stable, reentrant atrial flutter induced in 12 conscious dogs using a sterile pericarditis model were studied and compared with the effects of quinidine (5 mg/kg intravenously) given on a different day in 10 of the same 12 dogs. The effects of these drugs on atrial excitability, the atrial effective refractory period and intraatrial conduction time measured during rapid atrial pacing performed during sinus rhythm were also compared. The mean NAPA and quinidine serum levels were 17.7 and 7.1 micrograms/ml, respectively. Both NAPA and quinidine immediately prolonged the atrial flutter cycle length in all dogs, from 118 +/- 15 to 141 +/- 18 ms and from 119 +/- 17 to 153 +/- 21 ms, respectively (both p less than 0.001), and then terminated atrial flutter in 11 of the 12 NAPA studies and in 6 of the 10 quinidine studies. Neither drug affected atrial excitability. Both NAPA and quinidine increased the atrial effective refractory period significantly, from 138 +/- 17 to 168 +/- 20 ms (p less than 0.001) and from 136 +/- 14 to 148 +/- 16 ms (p less than 0.01), respectively. NAPA did not change intraatrial conduction time measured during atrial pacing at 150 beats/min, but during atrial pacing at 300 beats/min, it prolonged it from 51 +/- 9 to 54 +/- 10 ms (p less than 0.05), and at 400 beats/min, from 52 +/- 10 to 64 +/- 13 ms (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Acecainide↗
PubMed1991

The surgical treatment of atrial fibrillation. II. Intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation.

Computerized mapping of atrial fibrillation was performed in animals and man. To study atrial fibrillation in a systematic manner, we developed a clinically relevant experimental model of atrial fibrillation. Chronic mitral regurgitation was created surgically in 25 dogs without opening the pericardium. After several months of chronic mitral regurgitation, the atria became enlarged and sustained atrial fibrillation could be induced by standard programmed electrical stimulation techniques. Computerized isochronous activation maps of the atria were recorded during atrial fibrillation from 208 bipolar electrodes simultaneously. In a parallel study, human atrial fibrillation was mapped with a separate 160-channel intraoperative mapping system in patients with paroxysmal atrial fibrillation who were undergoing surgical correction of the Wolff-Parkinson-White syndrome. The canine activation sequence maps demonstrated a spectrum of rhythm abnormalities ranging from simple atrial flutter to complex atrial fibrillation. They also showed that macroreentrant circuits within the atrial myocardium were responsible for the entire spectrum of arrhythmias. Atrial reentry was also documented during human atrial fibrillation. All patients had nonuniform conduction around regions of bidirectional block in both atria resulting in multiple discrete wave fronts. In addition, six patients had a single reentrant circuit in the right atrium in which bidirectional block of the activation wave front occurred along the sulcus terminals between the venae cavae. The left atrium in all patients demonstrated multiple wave fronts and conduction block, but left atrial reentry could not be detected. Both the experimental study and the clinical study demonstrated that multiple wave fronts, nonuniform conduction, bidirectional block, and large (macroreentrant) reentrant circuits occur during atrial fibrillation. The presence of macroreentrant circuits and the absence of either microreentrant circuits or evidence of atrial automaticity suggests that atrial fibrillation should be amenable to surgical ablation.

Adult↗
PubMed1992

The alternation between atrial flutter and atrial fibrillation.

Atrial fibrillation and atrial flutter share a common reentrant mechanism. However, the relationship between these arrhythmias has not been systemically studied to date. To evaluate the degree to which these arrhythmias may alternate, consecutive Holter monitor recordings which showed fibrillation or flutter in 96 patients were reviewed. One half of the patients were studied after open-heart surgery and the other half for varying indications. One quarter of the patients had atrial flutter in addition to fibrillation, and this alternation with flutter was significantly associated with the use of a type 1A antiarrhythmic drug (p = 0.007), but not with the use of digoxin or beta blockers (p = NS for both). Furthermore, this alternation with flutter was more common in the postoperative group (p = 0.01). A history of embolization was less common in patients who were in the postoperative group (p = 0.003) and patients who had flutter in addition to fibrillation (p = 0.05).

Adolescent↗
PubMed1991

The surgical treatment of atrial fibrillation. I. Summary of the current concepts of the mechanisms of atrial flutter and atrial fibrillation.

Atrial fibrillation is a common arrhythmia that is frequently resistant to medical therapy and has no satisfactory surgical therapy. The development of an effective surgical procedure to treat atrial fibrillation has been hampered by the paucity of clinically relevant information on the basic mechanisms responsible for the arrhythmia. This paper summarizes the current concepts of the electrophysiologic abnormalities in atrial flutter and fibrillation.

Animals↗
PubMed1992

Pharmacologic suppression of atrial flutter induced by atrial stimulation.

To examine the electrophysiologic properties of human atrial flutter and its response to various classes of antiarrhythmic drugs, 39 patients were identified as having inducible sustained atrial flutter with atrial extra-stimulation techniques. Measurement of intra-atrial, interatrial, atrioventricular node and His-Purkinje-conduction intervals, atrial refractory periods, and atrial flutter-cycle length were made before and after intravenous administration of verapamil, ouabain, or cedilanid, propranolol, and procainamide in these 39 patients, as well as in seven control patients. Verapamil significantly shortened flutter-cycle length but suppressed atrial-flutter induction in only one of seven patients. Two of nine patients who received propranolol proved resistant to flutter provocation; the seven patients who remained nonsuppressible exhibited greater prolongation of interatrial-conduction time. Ouabain and cedilanid suppressed flutter inducibility in four of seven patients, and flutter-cycle length increased in those patients remaining inducible. Procainamide suppressed flutter induction in nine of 11 patients. These results suggest that procainamide is the most effective agent of those agents tested in suppressing atrial flutter induced by atrial extra-stimulation. Verapamil and propranolol proved quite ineffective in suppressing inducible atrial flutter.

Adult↗
PubMed1978

Dual echocardiographic determination of atrial contraction sequence in atrial flutter and other related atrial arrhythmias.

We have applied the new technique of dual echocardiography to determine the sequence of atrial contraction as reflected in the simultaneously recorded movements of the tricuspid and mitral valves. The study group included 29 normal subjects and 23 patients with either atrial flutter, coarse atrial fibrillation or atrial tachycardia with block. In normal individuals, right atrial contraction preceded left atrial contraction, with an average interatrial contraction time of 17 +/- 8 msec. In contrast, the atrial contraction sequence was reversed in atrial flutter, with left preceding right atrial contraction and a prolonged interatrial contraction time of 82 +/- 20 msec. In two patients with atrial tachycardia with block, atrial contraction was either simultaneous or left preceded right atrial contraction by a brief interval. The sequence of atrial excitation, as determined by electrode catheter recordings from the right and left atria in one patient with atrial flutter and one patient with normal sinus rhythm, was the same as the contraction sequence. Left atrial pacing reversed both excitation and contraction sequences. After cardioversion of three patients from atrial flutter to normal sinus rhythm, interatrial contraction time was shortened but remained longer than in normal subjects, suggesting an interatrial conduction disturbance in patients with atrial flutter. In coarse atrial fibrillation, the contraction sequence varied. Significant motion of both mitral and tricuspid valves coincident with fibrillary waves occurred frequently, especially when the fibrillary waves were coarse and regular. Dual echocardiography permits the noninvasive determination of the sequence of atrial contraction and excitation, and may be useful in studying the characteristics of atrial arrhythmias.

Atrial Fibrillation↗
PubMed1992

Activation patterns in experimental canine atrial flutter produced by right atrial crush injury.

OBJECTIVES: This study was designed to localize and characterize the atrial flutter reentrant circuit and the electrophysiologic effects of right atrial crush injury in a new canine model. BACKGROUND: In previous studies sustained atrial flutter was induced in the canine heart by rapid atrial pacing after a linear crush injury was placed in the right atrial free wall. METHODS: Eight dogs (group 1) with three electrode plaques on the right and left atria and Bachmann's bundle and seven dogs (group 2) with a single high density electrode plaque on the right atrium were studied with use of a 64-channel computerized mapping system. RESULTS: At baseline, during sinus rhythm and right and left atrial pacing, activation spread uniformly without areas of slow conduction. Crush injury produced marked conduction delay or complete block during sinus rhythm, increasing the mean difference in activation times across the injury compared with control values (group 1, 31 +/- 4 vs. 14 +/- 5 ms, p less than 0.01; group 2, 28 +/- 10 vs. 7 +/- 2 ms, p less than 0.01). Rapid atrial pacing (S1S1 200 ms) above and below the crush injury revealed a line of complete block across which adjacent electrodes recorded markedly different activation times (33 +/- 5 and 38 +/- 12 ms difference, respectively) and around which activation wave fronts proceeded, colliding opposite the stimulating electrodes. The mean atrial flutter cycle length of 11 episodes induced in group 1 and 14 episodes in group 2 was 157 +/- 16 and 140 +/- 16 ms, respectively (p = NS). Activation mapping revealed a reentrant circuit in the right atrium around the crush injury in all episodes. Although the reentrant circuit did not contain a discrete area of slow conduction, activation time below was longer than that above the crush injury (92 +/- 14 vs. 66 +/- 8 ms and 82 +/- 12 vs. 59 +/- 9 ms in groups 1 and 2, respectively, p less than 0.01 for both). Rapid atrial pacing or premature stimuli produced progressive conduction delay and unidirectional block between the crush injury and the tricuspid anulus, inducing atrial flutter directly in 9 of 25 episodes. In 16 episodes, atrial flutter developed after transient induction of atrial fibrillation. CONCLUSIONS: 1) Atrial flutter in this model is due to reentry in the right atrium; 2) the crush injury functions as an anatomic obstacle around which reentry may occur; and 3) the reentrant circuit does not contain a discrete area of slow conduction but, rather, generally slower conduction below the crush injury.

Animals↗
PubMed1990

[A mechanism of terminating atrial flutter using programmed atrial stimulation].

The analysis of 1168 programmed stimulations (PS) from 30 studies during the last 20 years has shown that the termination of atrial flutter (a-flut) by means of PS directly resulted in sinusrhythm (SR) in 45% of cases. SR following a brief atrial fibrillation (a-fib) occurs in 20% of cases, while in 30% of cases a permanent a-fib results. Our study of 107 cases of a-flut have confirmed these results. The technique of stimulation and the atrial rate show no difference in how the result groups are distributed. It seems as if the maximal pacing rates applied play an important role in whether SR or a-fib is brought about. Permanent a-fib was more often the result of a high pacing rate. A comparable relationship is valid for the difference between the a-flut rate and the maximal pacing rate employed. There was no relation to the pacing rate whether SR was achieved directly or after a brief a-fib. The pacing rate and the difference was equally great when the a-flut was terminated into both groups, but significantly less then when permanent a-fib was triggered. There are three possible mechanisms which may be used to explain how an interaction between programmed stimulation and reentry could take place.

Adult↗
PubMed1992

Mechanism of double potentials recorded during sustained atrial flutter in the canine right atrial crush-injury model.

BACKGROUND: During atrial flutter, double potentials may be recorded at specific sites in the atria. It has been suggested that double potentials represent sequential activations at the center of the reentrant circuit. An alternative hypothesis is that double potentials represent electrical activity in an area of slow conduction. Understanding their mechanism is important because double potentials have been considered a possible indicator of target sites for catheter ablation. METHODS AND RESULTS: We systematically studied double potentials in our canine model of atrial flutter produced by right atrial crush injury using a 64-channel computerized mapping system with 56 electrodes on the right atrium in seven mongrel dogs under general anesthesia. Activation maps were recorded during sinus rhythm before and after crush injury, during rapid pacing above and below the crush injury, and during sustained atrial flutter, entrainment of atrial flutter, and termination of atrial flutter induced with D-sotalol (2 mg/kg). During sinus rhythm before crush injury, activation was uniform, and double potentials were not recorded in any dog. After crush injury, activation proceeded up to and around the crush injury, and narrowly split double potentials were recorded in two of seven dogs. During rapid pacing above and below the crush injury, double potentials were recorded in five dogs. During 14 episodes of atrial flutter (mean cycle length, 140 +/- 16 msec), double potentials were recorded at electrodes along the crush injury. The activation time of the early x component of the double potentials (25 +/- 13 msec) was similar to that of adjacent electrodes above the crush injury (24 +/- 11 msec), and the activation time of the late y component (89 +/- 13 msec) was similar to that of adjacent electrodes below the crush injury (91 +/- 14 msec). The timing of the x and y components was dependent on the location of the recording electrode, with x and y widely spaced at the end of the crush injury near the area of earliest atrial activation during atrial flutter, more equally timed at the center of the crush injury, and more closely timed at the end of the crush injury opposite the area of earliest activation. During transient entrainment, double potentials were accelerated to the pacing rate, but their activation time relative to adjacent electrodes was maintained. During abrupt termination of atrial flutter, the early x component of the double potential was always recorded, but the late y component was not, because of conduction block below the posterior end of the crush injury. CONCLUSIONS: This study has shown in our canine model of atrial flutter that double potentials are recorded from the center of the reentrant circuit and that they represent sequential activations as the reentrant wave front passes on either side of the crush injury.

Action Potentials↗
PubMed1991

Study on the genesis of the double potential recorded in the high right atrium in atrial flutter and its role in the reentry circuit of atrial flutter.

To investigate the genesis of the double potential (DP), which is two separate waves, and its role in the reentry circuit of atrial flutter (AF), we performed overdrive pacing (ODP) from the high right atrium (HRA) in six cases of spontaneous AF in which the DP was recorded in the HRA. In four of the six cases, when the DP was arbitrarily designated D1 and D2, D1 and D2 showed progressive fusion during ODP. In addition, the D1 return cycle, immediately after the termination of ODP, corresponded to the AF cycle, and the D2 return cycle corresponded to the pacing cycle. This may indicate that the DP is caused by the collision of two directional waves. Furthermore, it is suggested that the HRA plays an important role in preventing a possible shortcutting of reentry waves and in stabilizing the reentry circuit of AF.

Action Potentials↗