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PubMed1988

Inducible atrial flutter after the Mustard repair of complete transposition of the great arteries.

Atrial flutter is a common postoperative arrhythmia in patients with complete transposition of the great arteries (d-TGA) after the Mustard repair. Sixty patients with d-TGA who had the Mustard repair were evaluated by electrophysiologic studies. Thirty-three (55%) had inducible sustained atrial flutter; 17 of them developed spontaneous clinical episodes of atrial flutter (clinical atrial flutter group) and 16 did not (nonclinical atrial flutter group). In 6 of the 17 patients (35%) with clinical inducible atrial flutter, the condition was first documented in the electrophysiologic laboratory with subsequent development of spontaneous clinical episodes. Catheter endocardial mapping, used to determine atrial activation sequences and and conduction intervals, revealed intraatrial conduction delays with late activation of the low atrial sites in all patients. Abnormalities of atrial refractoriness were present, with a greater dispersion of atrial refractoriness found in the clinical atrial flutter group. Severe abnormalities of sinus nodal function appeared to a significantly greater degree among patients who had clinical episodes of atrial flutter. These electrophysiologic abnormalities and associated arrhythmias may predispose patients with d-TGA to sudden death.

Atrial Flutter↗
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↗
PubMed1975

Echocardiographic findings in atrial flutter.

Echocardiographic studies were performed in 22 patients with atrial fibrillation and atrial flutter. In atrial flutter, the echocardiograms consistently demonstrated regular undulatory waves of the posterior left atrial wall and upper left interventricular septum coinciding with each flutter wave of the electrocardiogram. The mitral valve was slightly reopened by each flutter wave occurring after diastolic mitral closure. The phonocardiogram simultaneously recorded with the echocardiogram showed only occasional atrial sounds. Coarse atrial fibrillation produced undulatory low frequency motion of both leaflets of the mitral valve during diastole. Atrial fibrillation with fine fibrillatory waves failed to show any significant and constant undulations of the left atrial wall and upper left interventricular septum. Echocardiographic evaluation of patients with atrial flutter could have diagnostic implications in doubtful cases with nondiagnostic electrocardiograms.

Adult↗
PubMed1996

Co-existence of atrial tachycardia and common atrial flutter: electrophysiological characteristics and radiofrequency catheter ablation.

Four patients, who had no prior atrial surgery, underwent radiofrequency ablation for clinically documented typical atrial flutter. In addition to typical atrial flutter re-entrant atrial tachycardia was initiated during electrophysiological study in these four patients. We used earliest atrial endocardial activation and concealed entrainment pace mapping with short stimulus-P interval (< 40 ms) to identify the exit site of slow conduction are of atrial flutter were located at the posteromedial right atrium between the coronary ostium and the tricuspid annulus and those of slow conduction area of atrial tachycardia were located at high lateral right atrium in all four patients. Radiofrequency energy applied to these exit sites successfully eliminated both atrial flutter and atrial tachycardia in these four patients. Typical atrial flutter and re-entrant atrial tachycardia with two distinct re-entrant circuits concomitantly occurring in patients without prior atrial surgery are rare. Radiofrequency ablation can abolish both atrial tachyarrhythmias in the same ablation session.

Aged↗
PubMed1998

Fetal atrial flutter: diagnosis, clinical features, treatment, and outcome.

OBJECTIVES: To assess clinical features, treatment efficacy, and outcome of fetal atrial flutter. STUDY DESIGN: All atrial flutter cases seen in our unit between 1988 and 1995 were reviewed retrospectively and compared with the pooled data of 37 echocardiographically documented and published cases. RESULTS: Atrial flutter was found in 15 of 49 (30.6%) fetuses who had been referred because of clinically relevant tachyarrhythmia. Mean age at detection was 34+/-4 weeks' gestation. Atrial flutter was incessant in 11 and intermittent in 4, with a mean atrial rate of 442+/-65 beats/min and a mean ventricular rate of 216+/-28 beats/min. A predominance of 2:1 atrioventricular conduction was observed. In 5 of 15 cases another form of arrhythmia (supraventricular tachycardia, chaotic atrial rhythm, ventricular extrasystoles) coexisted with atrial flutter. Eleven fetuses were treated with maternal digoxin, and five subsequently converted to sinus rhythm. Four fetuses received no medication; of these four, two showed brief self-limited episodes of atrial flutter and two were delivered after detection of the arrhythmia. Only one fetus (6.7%), who did not respond to drug therapy, was delivered prematurely because of mild congestive heart failure. Seven neonates were in atrial flutter at birth; rhythm control could be easily achieved with sotalol or digoxin (n = 5), flecainide (n = 1), or electroconversion (n = 1) within the first 2 days of life without any relapse. CONCLUSION: Fetal atrial flutter accounts for approximately one third of all clinically relevant tachyarrhythmia. Although the suppression rate of incessant atrial flutter with digoxin is only 50%, this therapy may be useful for its positive inotropic and negative chronotropic properties. In our experience most fetuses with therapy-resistant atrial flutter and absence of 1:1 atrioventricular conduction do not experience congestive heart failure and do not need to be delivered prematurely. After birth, conversion to sinus rhythm was easily achieved in all neonates.

Anti-Arrhythmia Agents↗
PubMed1993

Association between atrioventricular node reentrant tachycardia and inducible atrial flutter.

OBJECTIVES: The purpose of this study was to evaluate the inducibility of atrial flutter in patients with atrioventricular (AV) node reentrant tachycardia and to determine the effect of radio-frequency ablation of the slow AV node pathway on the inducibility of atrial flutter. BACKGROUND: Studies have shown that both AV node reentrant tachycardia and atrial flutter are reentrant arrhythmias having an area of slow conduction that is located in the low posterior right atrium near the ostium of the coronary sinus. METHODS: Ninety-one patients were prospectively evaluated using a standardized atrial pacing protocol. Three groups of patients were analyzed: 42 patients with inducible AV node reentrant tachycardia, 13 with a history of spontaneous atrial flutter and 36 control patients. A subgroup of 34 patients with AV node reentrant tachycardia who underwent successful radiofrequency ablation of the slow AV node pathway underwent atrial pacing again after ablation. RESULTS: Atrial flutter was more frequently inducible in patients with AV node reentrant tachycardia (88%) and in those with a history of atrial flutter (92%) than in control patients (36%) (p = 0.0001). There were no differences between the patient groups with respect to atrial effective refractory period, P wave duration or PA interval at the His position. Among the 34 patients with AV node reentrant tachycardia who underwent atrial pacing before and after radiofrequency ablation, there were 30 with atrial flutter and 4 with atrial fibrillation before ablation and 29 with atrial flutter and 5 with atrial fibrillation after ablation (p = NS). There was no difference in the duration of the induced atrial flutter before and after ablation. The mean atrial flutter cycle length before ablation (206 +/- 22 ms) was not different from that after ablation (196 +/- 20 ms) (p = NS). CONCLUSIONS: There is a strong association between AV node reentrant tachycardia and inducible atrial flutter, suggesting that there may be a common area of perinodal atrium participating in the two tachycardia circuits. However, radiofrequency ablation of the slow pathway of the AV node reentrant tachycardia circuit does not influence the inducibility of atrial flutter.

Adult↗
PubMed1994

Catheter ablation of atrial flutter using radiofrequency energy.

Sixteen patients with type I atrial flutter underwent an attempt at radiofrequency catheter ablation (8 women, 8 men, mean age 53 +/- 11 years). The primary criterion used to identify sites for radiofrequency energy delivery was the identification of a fractionated electrogram. Radiofrequency energy was delivered for 20 to 30 seconds. Radiofrequency catheter ablation was acutely successful in 13 patients and unsuccessful in 3. During a mean follow-up of 10 +/- 4 months, 9 of 13 patients with a successful acute result (69%) remained free of recurrent atrial flutter or atrial fibrillation. The ability to induce nonclinical types of atrial flutter was associated with an unsuccessful outcome. A greater proportion of electrograms recorded at successful sites demonstrated electrogram stability compared with unsuccessful ablation sites. None of the electrograms recorded at successful ablation sites were fractionated or had a double potential. This study demonstrates that radiofrequency catheter ablation of type I atrial flutter can be achieved safely.

Adult↗
PubMed1989

[A-V conduction in atrial flutter. Electrocardiographic study].

One hundred and twenty-nine cases of atrial flutter were analyzed to assess the A-V conduction. The R-R intervals, the A-V conduction ratio, and the F-R intervals were measured in each case. Conduction in atrial flutter was defined either as constant or as variable depending on whether the A-V conduction ratio was fixed or variable. Furthermore, atrial flutter was defined as regular whenever the R-R intervals were mathematically related to each other, any interval being a multiple of the F-F cycle. On the other hand, atrial flutter was defined as irregular when the R-R cycles did not reflect a precise mathematical relationship. The R-R intervals in irregular atrial flutter were not exactly multiples of the F-F cycle. This was because the F-R intervals were variable. Sixty-five cases of atrial flutter had constant A-V conduction, whereas 64 cases were associated with variable A-V conduction. Eighty-eight per cent of cases with constant conduction were regular. On the contrary, 91% of cases with variable A-V conduction were irregular. These data reflect a relationship between the constancy of the A-V conduction ratio and the regularity of the R-R intervals. Several mechanisms were identified as being responsible for atrial flutter irregularity. Alternation of the F-R intervals was the most frequent mechanism leading to irregularity of atrial flutter with constant A-V conduction. Alternating Wenckebach periodicity was the most common cause of irregularity in atrial flutter with variable conduction ratio. Concealed conduction of blocked impulses was also frequently involved in determining atrial flutter irregularity.

Atrial Flutter↗
PubMed1999

What is the relationship of atrial flutter and fibrillation?

Animal models and human studies of atrial activation mapping and entrainment have considerably enhanced our understanding of the anatomical substrate for atrial flutter and created the basis for a definite cure with radiofrequency catheter ablation. As atrial flutter has now become a curable arrhythmia, emphasis is shifting to understand the most common arrhythmia: atrial fibrillation. Furthermore, from clinical observation, it is apparent that there is a relationship between atrial fibrillation and atrial flutter in patients with atrial arrhythmias. Techniques that have informed our understanding of the anatomical basis of atrial flutter may also be useful in understanding the relationship between atrial fibrillation and flutter, including animal models, clinical endocardial mapping, and intracardiac anatomical imaging. Thus, atrial anatomy and its relationship to electrophysiological findings, and the role of partial or complete conduction barriers around which reentry can and cannot occur, may be of importance for atrial fibrillation as well. Ultimately, the relationship between atrial fibrillation and atrial flutter may inform our understanding of the mechanisms of atrial fibrillation itself, and help to develop new approaches to device, catheter-based, and pharmacological therapy for atrial fibrillation.

Animals↗
PubMed2006

[Typical atrial flutter: history, mechanisms and radiofrequency "ablation"].

yipical atrial flutter can now be permanently cured by a single session of radiofrequency ablation, a non pharmacological technique. The term "atrial flutter" is in fact somewhat confusing. A review of the history of this form of tachycardia shows that atrial flutter is indeed a multiple entity. While the reentrant nature of atrial flutter has long been known, most cardiologists refer to the typical ECG aspect and right atrial macro reentry circuit with counterclockwise rotation, as described by Puech. It is now possible to classify these flutters according to their electrocardiographic aspect and electrophysiological mechanisms. This article describes the diagnostic signs of typical flutter, and provides a detailed description of the most frequently used radical therapy, namely catheter ablation of the cavotricuspidian isthmus. This technique delivers radiofrequency pulses, under continuous local temperature monitoring, in order to permanently interrupt conduction in this structure. Outcome is assessed with the pacing technique and local electrocardiography. In experienced hands the immediate success rate is very high, late recurrence is rare, and complications are virtually absent.

Atrial Flutter↗
PubMed1993

Antiarrhythmic and electrophysiologic effects of ibutilide in a chronic canine model of atrial flutter.

We studied the effects of orally administered ibutilide, a class III antiarrhythmic agent, in a model of reentrant atrial flutter in conscious dogs. After baseline determination of atrial effective refractory period (AERP) and demonstration of reproducible induction of atrial flutter by rapid atrial pacing, 8 dogs received either placebo or one of six doses of ibutilide ranging from 0.1 to 5 mg/kg. Refractory periods and the ability to induce atrial flutter were then assessed at periodic intervals for 8 hours. Ibutilide produced dose-related increases in AERP which were well correlated with prevention of initiation of atrial flutter after doses > or = 0.25 mg/kg. Placebo and 0.1 mg/kg ibutilide had no effect on AERP or the ability to induce atrial flutter. Doses of 0.25 to 1.0 mg/kg ibutilide significantly increased AERP and prevented induction of atrial flutter for 4-6 h. After treatment with 2.5 or 5 mg/kg ibutilide, significant increases in AERP and prevention of induction of atrial flutter persisted throughout the 8-h study period. The cycle length of inducible atrial flutter was significantly increased after administration of 5 mg/kg ibutilide. The results demonstrate oral efficacy of ibutilide with rapid onset of action (in 30-60 min), resulting in increased AERP and prevention of induced atrial flutter in this model.

Administration, Oral↗
PubMed1996

Radiofrequency ablation of atrial flutter.

Activation mapping in common atrial flutter has shown circular (reentrant) activation of the right atrium around anatomic structures and areas of functional block. The direction of rotation is counterclockwise (in a frontal view), and in the low right atrium the myocardium between the inferior vena cava (IVC) and the tricuspid valve (TV) is critical to close the activation circle. The circuit can be interrupted by radiofrequency ablation of the myocardium between the TV and the IVC, and, in some cases, by ablation between the coronary sinus and TV. Flutter interruption does not mean complete isthmus ablation, as it may remain inducible, requiring further ablation. Despite attaining noninducibility, flutter may recur, and new procedures may be needed for complete ablation. Atrial fibrillation occurs in up to 30% of the cases during follow-up but is generally well controlled with antiarrhythmic drugs that were ineffective in treating flutter before ablation. Some noncommon atrial flutters show circular right atrial activation in a reversed (clockwise) direction, with the same critical areas in the low right atrium, and in these isthmus ablation is effective. Other noncommon flutters have different substrates in the right or left atrium, and mapping has to define specific critical isthmuses as ablation targets in each case. Left atrial flutter circuits remain inaccessible to ablation.

Atrial Fibrillation↗
PubMedDate not supplied

Radiofrequency catheter ablation of common atrial flutter--acute and follow-up results.

Atrial flutter with a structurally well-defined macro-reentrant circuit in the right atrium has recently become amenable to radiofrequency ablation with the recognition of isthmus as a narrow zone of slow conduction. This study describes 20 consecutive and symptomatic patients with atrial flutter (15 males, 5 females; mean age 38.5 +/- 10.2 years) who underwent radiofrequency ablation in our institute in the last 18 months. Fourteen patients had structurally normal hearts, while the remaining six patients had specific disorders (prior surgery for closure of atrial septal defect-2, idiopathic restrictive cardiomyopathy-1, primary sinus node dysfunction-2, tachycardiomyopathy-1). The endpoints of a complete isthmus block and conversion to sinus rhythm were achieved in 19 of the 20 patients. Total number of pulses needed to attain the endpoints was a mean of 4.2 (range 1-5), each pulse being delivered for 90 seconds. At a mean follow up of 9.4 +/- 3.2 months (range 6-12 months), recurrence of atrial flutter was seen in one patient, atrial fibrillation in two and sinus node reentrant tachycardia in one. These results are comparable to those reported in the literature. Achievement of a complete isthmus block appears to be an important endpoint in obtaining optimal results. The issues of alternative sites of ablation, long-term results and advantages of an 8 mm tip catheter need to be examined further. In conclusion, radiofrequency ablation appears to be the preferred mode of treatment for patients with atrial flutter with excellent short-term and mid-term results.

Adolescent↗
PubMed1994

Ventricular beats induce variations in cycle length of rapid (type II) atrial flutter in humans. Evidence of leading circle reentry.

BACKGROUND: Slight variation in cycle lengths of common and rapid atrial flutter in humans is an established phenomenon, but its mechanisms have not been completely clarified. In a previous study, we demonstrated that in common atrial flutter the variations in atrial cycle length were due to atrial stretch affecting the revolution time of a reentrant circuit. In the present study, we investigate the nature of atrial cycle length variations in the rapid type of human atrial flutter. METHODS AND RESULTS: Atrial interval variations of 17 episodes of rapid atrial flutter in 14 patients were investigated by measuring the sequence of atrial intervals from intraesophageal or intra-atrial leads and the onset of QRS complexes from a surface lead (V1). To study whether interval variation in flutter cycle was related to ventricular activity, a phase plot was constructed in which the flutter cycle length was plotted against the time after the previous QRS complex. This showed that the interval fluctuations were strictly coupled to the moment of ventricular activation. After the onset of the QRS complex, the rapid atrial flutter interval gradually decreased by an average of 4.1% (P < .001) and reached a minimum value after 300 to 600 milliseconds. Thereafter, the intervals increased again until the next ventricular beat occurred. In 10 patients developing both common and rapid atrial flutter, two different phase relations were found. Whereas during common atrial flutter the atrial interval increased after the QRS complex, it decreased during rapid atrial flutter. In three patients, intra-atrial pressure was recorded together with the electrical activity during both common and rapid atrial flutter episodes. This showed that variations in atrial flutter cycle length were associated with the rise of atrial pressure during ventricular contraction. CONCLUSIONS: These findings indicate a role of contraction-excitation feedback caused by atrial stretch after a ventricular activation. The shortening of the atrial interval after the onset of the QRS complex as found in patients during rapid atrial flutter can be explained by stretch-induced shortening of atrial refractoriness and consequent shortening of the revolution time of a functionally determined intra-atrial circuit.

Aged↗
PubMed1979

Atrial flutter with exit block.

The mechanism of atrial flutter is controversial. A 76-year-old woman with rheumatic heart disease was referred to our clinic with an unusual rhythm disturbance which initially appeared to be classic atrial flutter at a rate of 300 beats/min. Later tracings, however, demonstrated a rate exactly one-half that of the earlier ECGs, with an identical p-wave morphology and vector. This latter rhythm also behaved in a manner expected for a flutter mechanism in that both spontaneously and with carotid pressure high-degree atrioventricular block occurred without alteration of the underlying atrial mechanism. Finally, the two rates interchanged spontaneously over several days without any significant interval changes in medical therapy. These findings were initially explained as probable digoxin toxicity. The underlying mechanism, however, was more likely atrial flutter with exit block and in this patient may have represented another facet of her sick sinus syndrome. This unusual phenomenon is discussed in terms of previous reports and possible implications for the mechanism of atrial flutter.

Aged↗
PubMed2000

The role of the crista terminalis in atrial flutter and fibrillation: a computer modeling study.

Although atrial fibrillation is a common arrhythmia, the underlying mechanisms are incompletely understood. Recent studies have determined the role of the crista terminalis in the mechanisms of a simpler arrhythmia, atrial flutter. We hypothesize that as transverse coupling across the crista terminalis increases, the activation pattern that results is less like typical atrial flutter and more like atrial fibrillation. 6480 Van Capelle elements were coupled in an icosahedron, simulating the right atrium. Atrial simulations were created which incorporated no heterogeneity, heterogeneous coupling, heterogeneous effective refractory periods, and both heterogeneous coupling and effective refractory periods. When the entire crista terminalis was uncoupled, typical atrial flutter occurred. When transverse coupling allowed activation to propagate across the crista terminalis, the flutter cycle length decreased (p<0.0001). In addition, when heterogeneity was present, both the coefficient of variation of cycle length and the number of activation wavelets increased (p<0.0001). Thus, a more rapid reentrant circuit in the superior right atrium drove fibrillatory activity in the remainder of the atrium, as predicted by the "mother wavelet hypothesis." While awaiting in vivo validation, our study indicates that transverse coupling along the crista terminalis may play an important role in the development of atrial fibrillation from atrial flutter.

Atrial Fibrillation↗
PubMed1994

Radiofrequency ablation of atrial flutter. Efficacy of an anatomically guided approach.

BACKGROUND: Previous reports have shown that radiofrequency ablation can terminate atrial flutter and prevent recurrences. However, different methods have been used, and the current experience remains limited. The objective of the present study was to determine the efficacy of radiofrequency ablation of atrial tissue in patients with atrial flutter using an anatomically guided approach. METHODS AND RESULTS: We treated 22 patients aged 30 to 73 years. Atrial flutter was recurrent for a mean of 5 years despite the administration of multiple antiarrhythmic drugs. Radiofrequency current was directed to the atrial isthmus between the inferior vena cava and the tricuspid ring, regardless of the morphology of local electrograms. Radiofrequency energy was applied during typical atrial flutter in 12 patients, atypical atrial flutter in 2 patients, and successively both forms in 8 patients. In 19 patients, atrial flutter abruptly terminated. In 3 patients, atrial flutter persisted despite 37, 48, and 25 applications, respectively. Atrial recordings demonstrated that atrial flutter termination occurred as a consequence of conduction block at the site of radiofrequency energy application, regardless of the type of atrial flutter. The number of applications before termination ranged from 1 to 82 (mean, 32). Atrial flutter could no longer be induced in every case. There were no complications. During a 13-month mean follow-up, atrial flutter recurred in only 2 of the 19 patients who had a successful ablation. Four patients experienced chronic atrial fibrillation, and 2 of them returned to sinus rhythm with antiarrhythmic therapy. CONCLUSIONS: Radiofrequency ablation of atrial flutter using anatomic guidance is feasible and effective. Further experience is needed to delineate its role as an alternative approach to the management of refractory atrial flutter.

Adult↗
PubMed1996

Combined transesophageal left atrial pacing and antiarrhythmic therapy in the treatment of atrial flutter.

In order to terminate atrial flutter (AF) overdrive transesophageal left atrial pacing (TELAP) was performed in 760 patients with paroxysmal AF. There were 315 women and 415 men (mean age 59 years). In 260 patients, TELAP was used in an outpatient setting. Approximately half of the patients (51%) had coronary artery disease and/or arterial hypertension, and 23% of the patients had no structural heart disease. The duration of AF ranged between 1 hour and 1 month. TELAP was performed in 312 patients without any antiarrhythmic drug (AAD) administration (group I) and in 448 patients after administration of AAD (procainamide and/or amiodarone) in conventional doses (group II). TELAP resulted in immediate return of sinus rhythm in 85 patients (27%) of group I and in 222 patients (50%) of group II (P < 0.001). TELAP converted AF to atrial fibrillation (AFIB) in 185 of group I and in 214 (48%) of the group II patients (P < 0.01). In addition, within 1-2 days after TELAP AFIB converted to sinus rhythm spontaneously or after AAD in 87 patients of group I (28%) and in 84 (19%) of the group II patients (P < 0.01). In general sinus rhythm was restored in 172 (55%) of the group I and in 306 (68%) of the group II patients (P < 0.005). AF was converted to AFIB in 98 (31%) of the group I and in 130 (29%) of the patients in group II patients (NS). TELAP was ineffective in 42 (13.5%) of the group I and in 12 (3%) of the group II patients (P < 0.001). TELAP was an effective noninvasive method for the treatment of recent onset AF. Our experience showed that after TELAP, sinus rhythm was restored in most of the patients with paroxysmal AF within 1-2 days. In some patients TELAP converted AF to AFIB, making it easier to control the heart rate with AAD. Treatment with AAD before TELAP increased its effectiveness.

Ambulatory Care↗