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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↗
PubMedDate not supplied

Atrial flutter.

Atrial flutter is a supraventricular tachydysrhythmia believed to arise from electrophysiologic disturbances in the atria. It tends to be an unstable rhythm and is usually associated with intrinsic cardiac or pulmonary disease or adverse extrinsic influences on the heart. It is due to either a reentry mechanism or an increased atrial automaticity. Atrial depolarization is regular at a rate of 260 to 340 beats per minute. With a normal atrioventricular (AV) node there is usually a physiologic second-degree block with resultant 2:1 conduction. Higher degrees of AV block can occur in patients with AV nodal disease, increased vagal tone, or when certain drugs are in use. One-to-one conduction may occur in patients with accessory AV nodal pathways. In this situation, serious adverse effects are often seen, including palpitations, dizziness, syncope, angina, and dyspnea. Electrical cardioversion is the safest and most reliable way of terminating atrial flutter and its use should not be delayed in an unstable patient. In the nonemergent situation a variety of medications alone or in combination can be used to convert the rhythm or slow ventricular response.

Atrial Flutter↗
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↗
PubMed1980

Conversion of atrial flutter: rapid atrial pacing as a bedside technique.

Eleven patients with atrial flutter underwent intracardiac right atrial pacing at bedside in an attempt to terminate this dysrhythmia. Nine of the eleven patients were converted to sinus rhythm; the remaining two patients were converted to atrial fibrillation with a slower ventricular rate. There were no complications. The potential hazards of direct current cardioversion (anesthesia, fractures, muscle strain, myocardial injury, etc.) were avoided. In contrast to rapid atrial pacing in the electrophysiology laboratory, the bedside technique did not require a special laboratory setting, electronic or x-ray equipment, or technical personnel. Transportation of critically ill patients was obviated. Atrial flutter can be converted at the bedside to a more favorable rhythm; the expediency, safety, and low cost of this bedside cardioversion technique not only makes it feasible, but also it is often the procedure of choice.

Adult↗
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↗
PubMed1985

[Atrial flutter and atrial fibrillation by DDD stimulation].

136 patients were followed after implantation a DDD pacemaker (PM) for a total of 1,919 patient-months (m = 14.1 months/patient). 22/136 patients had one or more episodes of atrial flutter or fibrillation (AF) postoperatively. In 121/136 patients (group A) AF had not been documented before, in 4 it was unknown at the time of implantation, but was verified retrospectively (group B). 11 patients (group C) had a positive history of previous AF. Post implantation 7.4% in group A and 81.8% in group C developed AF. In patients with sick sinus syndrome (SSS) the incidence was 10/37 (27%), in those with AV block (AV) 6/77 (7.8%) and in cases with both SSS and AV 6/22 (27.3%). The first AF episode occurred during the implantation itself (n = 2) or during the hospital course in 9/22 patients (A: 11%, B/C: 64% early attacks), and later on in 13 with a time delay of 1-24 months (m = 8.5, 8 patients) in group A and 2-15 months (m = 6.6, 4 patients) in groups B/C. 2 patients of group C had no AF episodes post implantation. In the individual patient the number of attacks ranged from 1 to 3 (10.4/100 patient-months) in group A and from 1 to 6 (20.1/100 patient-months) in groups B/C. During AF 16/22 patients had a ventricular rate of 110-185, m = 132 bpm. In 6 patients the tachycardia was mediated by the PM and in 10 by fast intrinsic AV conduction. 1 patient with SSS, 2 with SSS + AV (spontaneous ventricular rate less than 45 bpm) and 3 with AV needed ventricular backup-pacing during AF. In 7 patients a total of 15 attacks of atrial flutter could be terminated by atrial overdrive pacing, in 5 of these episodes by temporary high rate A00 stimulation via the implanted pacemaker lead system. Otherwise AF was converted to sinus rhythm by antiarrhythmic drugs. After termination AF often recurred, but only 3 patients developed chronic atrial fibrillation. In 2 patients a ventricular rate greater than 180 bpm during AF reverted the PM to asynchronous mode, a possible cause of ventricular fibrillation in one. No other complications due to the PM itself have been encountered. AF, therefore, common during DDD pacing, even in patients without any AF history before implant. Both the incidence and the recurrence of AF depend on the presence or absence of previous atrial arrhythmias.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
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↗