Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Atrial Flutter”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources

Neonatal intractable atrial flutter successfully treated with intravenous flecainide.

We present a neonatal case with intractable atrial flutter that did not respond to digitalization and electrical cardioversion. Intravenous flecainide administration completely resolved the atrial flutter. Proarrhythmic effects were not induced by flecainide administration. Although the efficacy of flecainide for atrial flutter during the infantile or childhood period is low, intravenous flecainide is worth consideration as a treatment for atrial flutter, even in intractable cases as described here, during the neonatal period.

Anti-Arrhythmia Agents↗

Direct conversion of atrial flutter to sinus rhythm with low-output, short-duration transesophageal atrial pacing.

BACKGROUND AND HYPOTHESIS: Transesophageal atrial pacing (TAP) is useful for terminating paroxysmal non-self terminating atrial flutter (PAF); however, high output pacing of long stimulus duration causes severe symptoms such as chest pain. The objective of this study was to investigate the effect of low-output, short-duration TAP on the conversion of PAF. METHODS: We applied low-output (within 15 mA with a pulse duration of 10 ms), short-duration (within 4 s) TAP in 31 patients (50 +/- 19 years) with PAF. Transesophageal pacing was delivered with 10 pulses of burst pacing at intervals that were 20 ms shorter than those of the flutter wave length. When the conversion was unsuccessful, we delivered 20 pulses of burst pacing. RESULTS: Sixteen patients (52%) were converted directly to sinus rhythm and 12 (38%) to atrial fibrillation. Transesophageal pacing was ineffective in 3 (10%) patients. The duration of atrial flutter, maximum flutter wave amplitude, effective pacing intervals, underlying heart diseases, and cardiac function were not different between patients who had direct conversion to sinus rhythm and those converted to atrial fibrillation. The patients who had direct conversion to sinus rhythm had longer flutter wave cycle lengths than those converted to atrial fibrillation (248 vs. 221 ms, p < 0.005). No patient had complications and complained of any symptoms. CONCLUSION: Low-output, short-duration TAP was useful to convert PAF directly to sinus rhythm without side effects.

Adolescent↗

Electrophysiologic characteristics and ablation of an atypical atrial flutter in the right atrium.

Subeustachian isthmus-dependent typical atrial flutter has been well studied. We demonstrate a case with atypical atrial flutter involving only the base of the right atrium around the inferior vena cava. Entrainment pacing and mapping studies documented a distinct circuit traversing the subeustachian isthmus, propagating through the posterobasal right atrium, and skirting the inferior vena cava. Successful radiofrequency ablation of the arrhythmia was accomplished by creating a linear lesion at the subeustachian isthmus. Mapping of the inferior vena cava region and the demonstration of concealed entrainment are essential steps in establishing the mechanism of the atypical atrial flutter.

Atrial Flutter↗

Effects of disopyramide on cycle length, effective refractory period and excitable gap of atrial flutter, and relation to arrhythmia termination by overdrive pacing.

The administration of class IA antiarrhythmic drugs facilities termination of atrial flutter by overdrive pacing. To investigate the electrophysiologic determinants of this effect, changes in the cycle length, the effective refractory period and the excitable gap of spontaneous type I atrial flutter were studied in 11 patients given intravenous disopyramide (3 mg/kg in 1 hour). After drug infusion, the cycle length of atrial flutter increased from 238 +/- 26 to 298 +/- 38 ms (+25%; p less than 0.001) and the effective refractory period prolonged from 169 +/- 19 to 192 +/- 25 ms (+14%; p less than 0.01). The excitable gap prolonged from 62 +/- 16 to 96 +/- 27 ms (+55%; p less than 0.001). Atrial flutter was terminated by overdrive pacing (mean cycle 203) in 10 of 11 patients; in 1 patient atrial fibrillation resulted after high rate stimulation. In the setting of an anatomically defined reentry circuit, as in type I atrial flutter, the administration of disopyramide prolongs both cycle length and refractory period. The finding of an increased excitable gap suggests that the drug exerts its prominent effect by depressing conduction velocity. A wider excitable gap allows easier penetration of the stimulus in the reentry circuit and accounts for the beneficial effects of type IA antiarrhythmic drugs on the termination of atrial flutter by overdrive pacing.

Aged↗

Mechanism and location of atrial flutter in transplanted hearts: observations during transient entrainment from distant sites.

OBJECTIVES: This study was designed to elucidate the location and mechanism of typical atrial flutter in the transplanted heart. BACKGROUND: Although the F wave morphology in atrial flutter is similar in nontransplanted and transplanted hearts, the surgical incision needed for the atrial anastomosis may create a distinct electrophysiologic substrate of atrial flutter. METHODS: Entrainment from the lateral wall of the right atrium and interatrial septum was used to determine the location of atrial flutter in five patients with a transplanted heart and six patients with a nontransplanted heart. The difference between the first postpacing interval (FPPI) and the flutter cycle length (FCL) was used as an index of proximity to the circuit. RESULTS: In the transplant group, the FPPI was equal to the FCL at sites located close to the tricuspid annulus (TA); the mean differences (+/-SD) were 1 +/- 5 and -1 +/- 2 ms at the lateral wall and interatrial septum, respectively. However, from sites close to the surgical incision at the lateral wall and at the interatrial septum, these differences were significantly longer (29 +/- 12 and 27 +/- 9 ms, respectively, p < 0.05). In the nontransplant group, the FPPI was similar to the FCL at points in the lateral wall and interatrial septum close to the TA (mean difference 7 +/- 6 and 6 +/- 11 ms, respectively) and at sites close to the crista terminalis (CT) in the lateral wall (mean difference 4 +/- 4 ms). However, in sites separated from the TA at the interatrial septum the difference was markedly longer (35 +/- 11 ms, p < 0.05). CONCLUSIONS: Atrial flutter in transplanted hearts may best be explained by macroreentry around the tricuspid ring. In non-transplanted hearts a different structure (perhaps the CT?) may be the basis for atrial flutter at the lateral wall.

Atrial Flutter↗

Atypical atrial flutter involving the isthmus between the right pulmonary veins and fossa ovalis.

Typical atrial flutter, counterclockwise or clockwise movement around the tricuspid annulus, has been well studied. However, the reentrant circuits in atypical atrial flutter are not well defined. A patient without a prior history of cardiac surgery who presented with incessant atypical atrial flutter is described. Activation mapping demonstrated a circular movement around the fossa ovalis in the interatrial septum. Entrainment mapping demonstrated a protected isthmus between the right pulmonary veins and the fossa ovalis. Radiofrequency ablation of this isthmus terminated atrial flutter without recurrence during the follow-up period.

Aged↗

Conduction properties of the inferior vena cava-tricuspid annular isthmus in patients with typical atrial flutter.

INTRODUCTION: A functional region of slow conduction located in the inferior right atrium has been postulated to be critical to the induction and maintenance of typical human atrial flutter. We reexamined the potential role of functional conduction delay in the annular isthmus between the tricuspid valve and the inferior vena cava; it is within this region that such delays have been postulated to occur, and where interruption of conduction by radiofrequency energy application has been shown to eliminate typical flutter. METHODS AND RESULTS: Thirty patients with type I atrial flutter (30 counterclockwise, 14 clockwise) were studied. Counterclockwise and clockwise isthmus activation times adjacent and parallel to the tricuspid valve were measured during three conditions: (1) atrial pacing in sinus rhythm, (2) atrial flutter, and (3) entrainment of atrial flutter. During pacing in sinus rhythm at progressively shorter cycle lengths, both counterclockwise and clockwise isthmus activation times remained unchanged; decremental conduction prior to flutter induction or loss of capture was not observed. Counterclockwise isthmus activation time did not significantly differ during flutter (68 +/- 23 msec), inferolateral tricuspid annulus pacing (71 +/- 23 msec), or entrainment of flutter (72 +/- 23 msec). Similarly, clockwise isthmus activation times did not significantly differ between flutter (65 +/- 22 msec), proximal coronary sinus pacing (73 +/- 21 msec), or entrainment of flutter (64 +/- 15 msec). CONCLUSION: Decremental conduction is not characteristic of activation through the isthmus when activation is assessed parallel and adjacent to the tricuspid annulus. Functional slowing or conduction delay does not develop in this region during typical atrial flutter.

Aged↗

Mode switching failure during atrial flutter: the '2:1 lock-in' phenomenon.

AIMS: To evaluate incidence and mechanism of a special form of automatic mode switching (MS) failure in patients with atrial flutter. METHODS AND RESULTS: Retrospectively the charts of 134 patients implanted with dual chamber pacemakers with MS algorithms were reviewed. Seven patients (5.2%) were identified that presented with sustained rapid ventricular pacing resulting from atrial flutter with failure of automatic MS. Since this form of MS failure implies 2:1 tracking of atrial flutter, it was coined '2:1 lock-in'. A theoretical timing model was developed to clarify the mechanism of this special form of MS failure. Prerequisites for the '2:1 lock-in' phenomenon are: (1). the sum of the AV delay and the post ventricular blanking (PVAB) must be longer than the cycle length of the atrial flutter, (2). the tachycardia detection rate must be higher than half the atrial flutter rate and (3). the maximum tracking rate (MTR) must be higher than half the atrial flutter rate. Recommendations for programming in order to avoid this specific form of MS failure are made accordingly and parallel algorithms for flutter detection are discussed. CONCLUSION: '2:1 lock-in' is a typical form of MS failure in patients with atrial flutter and the mechanism is closely linked to the typical atrial sensing windows.

Algorithms↗

Electrophysiological and antiarrhythmic effects of the atrial selective 5-HT(4) receptor antagonist RS-100302 in experimental atrial flutter and fibrillation.

BACKGROUND: Stimulation of 5-HT(4) receptors increases atrial chronotropic and inotropic responses. Whether other electrophysiological effects are produced is unknown. In humans and swine, 5-HT(4) receptors are present only in atrium. Therefore, the effects of a novel 5-HT(4) receptor antagonist, RS-100302, and the partial agonist cisapride on atrial flutter and fibrillation induced in swine were studied to delineate the role of the 5-HT(4) receptor in modulating atrial electrophysiological properties and the antiarrhythmic potential of RS-100302. METHODS AND RESULTS: In 17 anesthetized, open-chest, juvenile pigs, atrial flutter or fibrillation was induced by rapid right atrial pacing with or without a right atrial free wall crush injury, respectively. Atrial effective refractory period (ERP), conduction velocity, wavelength, and dispersion of refractoriness were determined during programmed stimulation via a 56-electrode mapping plaque sutured to the right atrial free wall. Ventricular electrophysiological parameters were also measured. All electrophysiological parameters were measured at baseline and after infusion of RS-100302 and cisapride. In the atrium, RS-100302 prolonged mean ERP (115+/-8 versus 146+/-7 ms, P<0.01) and wavelength (8.3+/-0.9 versus 9.9+/-0.8 cm, P<0.01), reduced dispersion of ERP (15+/-5 versus 8+/-1 ms, P<0.01), and minimally slowed conduction velocity (72+/-4 versus 67+/-5 cm/s, P<0.01). These effects were all partially reversed by cisapride. RS-100302 produced no ventricular electrophysiological effects. RS-100302 terminated atrial flutter in 6 of 8 animals and atrial fibrillation in 8 of 9 animals and prevented reinduction of sustained tachycardia in all animals. CONCLUSIONS: The electrophysiological profile of RS-100302 suggests that it may have atrial antiarrhythmic potential without producing ventricular proarrhythmic effects.

Animals↗

Atrial flutter ablation using a technique for detection of conduction block within the posterior isthmus.

Catheter ablation orientated on the induction of a functional intraatrial block within the posterior isthmus of the tricuspid annulus has been shown to effectively abolish atrial flutter. In order to improve and simplify the current technique, a strategy based on an electrode catheter for combined right atrial and coronary sinus mapping and stimulation was explored prospectively. Twenty-four consecutive patients referred for catheter ablation of recurrent type I atrial flutter were included. A steerable 7 Fr catheter (Medtronic/Cardiorhythm) composed of two segments with 20 electrodes was used for right atrial and coronary sinus activation mapping and stimulation. Multiple steering mechanisms allowing intubation and positioning of the distal part within the coronary sinus were incorporated into the device. Adequate positioning of the mapping catheter was achieved solely via a transfemoral approach in all patients after 7.7 +/- 4.6 minutes, providing stable electrogram recordings during the entire ablation procedure. Radiofrequency current ablation (16.3 +/- 9.6 pulses) caused a significant bidirectional increase of the mean intraatrial conduction times via the posterior isthmus irrespective to the stimulation interval. Significant changes of intraatrial conduction properties were induced during ablation in 22 of 24 patients (bidirectional block: n = 18, unidirectional block: n = 3, conduction delay: n = 1, unchanged conduction: n = 2). Following ablation atrial flutter was noninducible in all patients. Twenty-two of 24 patients (92%) remained free of atrial flutter episodes during a follow-up of 12.5 +/- 5.7 months. Two of six patients without a bidirectional conduction block had a recurrence of atrial flutter. Atrial flutter ablation guided by the induction of an intraatrial conduction block can be effectively performed with this novel strategy for combined mapping of the posterior tricuspid isthmus, including coronary sinus and right atrial free wall. This transfemoral approach has a high accuracy with respect to the detection of radiofrequency current-induced changes of intraatrial conduction patterns.

Atrial Flutter↗

Atrial flutter in the fetus and young infant: an association with accessory connections.

OBJECTIVE: To highlight the association between atrial flutter and accessory connections in the fetus and young infant. DESIGN: A retrospective review from January 1985 to January 1990. PATIENTS: Fetuses, neonates, and young infants with atrial flutter. RESULTS: Four fetuses and five infants presented with atrial flutter. In two fetuses and one infant sinus rhythm returned spontaneously. The other six required cardioversion. Three of them developed orthodromic atrioventricular re-entry tachycardia and each had evidence of an accessory connection. CONCLUSIONS: Because atrial flutter in the fetus and neonate is rare, the high incidence of accessory connections in this group points to a possible aetiology of "idiopathic" atrial flutter in this age group.

Atrial Flutter↗

Delayed restoration of atrial function after conversion of atrial flutter by pacing or electrical cardioversion.

It is often suggested but never proven that atrial function is not affected during atrial flutter, nor after its conversion to normal sinus rhythm. To evaluate this hypothesis, a prospective study was performed in 22 patients (age range 20 to 88 years) with atrial flutter. Diastolic transmitral flow was analyzed with echo-Doppler before and after conversion. After randomization, conversion was attempted with overdrive pacing or up to two 50 J shocks. If the initial method was unsuccessful, a 200 J shock was administered. All patients were converted to sinus rhythm with this protocol. Shortly after conversion (at 1 and 6 hours), atrial contribution to ventricular filling was absent in 4 of 22 patients. In the remaining 18 patients, atrial contribution to ventricular filling was small. Atrial contribution to transmitral flow improved from 20 to 27% within 24 hours (p < 0.01) and increased further to 38% at 6 weeks (p < 0.005). Peak velocity of late diastolic filling increased from 0.28 m/s after 1 hour to 0.39 m/s after 24 hours (p < 0.0001) and improved even further during later follow-up. In 1 patient, an effective atrial systole was not observed until the 14th day. Cardiac output did not change significantly during the study period. No differences were observed between the conversion modalities. In conclusion, atrial dysfunction is present immediately after conversion of atrial flutter to normal sinus rhythm. This dysfunction occurs also after overdrive pacing and can last > 1 week. The findings suggest that stasis in the atria can remain temporarily present after successful conversion of atrial flutter to sinus rhythm.

Adult↗

Remodeling of sinus node function after catheter ablation of right atrial flutter.

INTRODUCTION: The purpose of this study was to investigate the effect of ablation of right atrial flutter upon sinus node function in humans. METHODS AND RESULTS: This study enrolled 35 patients. Twenty-four patients (16 men and 8 women; age 68 +/- 11 years) were referred for ablation of persistent atrial flutter (duration 8 +/- 11 months). After ablation, there was abnormal sinus node function defined as a corrected sinus node recovery time (CSNRT) > or = 550 msec. The control group consisted of 11 patients who were undergoing pacemaker implantation for sinus node disease but did not have a history of atrial dysrhythmias or ablation. Within 24 hours of ablation or pacemaker implantation, baseline maximal CSNRT was measured through a permanent pacemaker by AAI pacing at six cycle lengths: 600, 550, 500, 450, 400, and 350 msec. CSNRT then was measured in the same manner at 48 hours, 14 days, and 3 months after ablation/pacemaker implantation. P wave amplitude and duration, and percent atrial sensing also were assessed at the same intervals. For patients undergoing atrial flutter ablation, there was progressive temporal recovery of CSNRT (1,204 +/- 671 msec at baseline vs 834 +/- 380 msec at 3 months; P < 0.001) and a significant increase in the percent atrial sensing and P wave amplitude at 3 months compared with baseline (P < 0.001). In control subjects, there was no change in the CSNRT, percent atrial pacing, or P wave amplitude. CONCLUSION: After ablation of persistent atrial flutter, there is temporal recovery of CSNRT and increase in spontaneous atrial activity. These findings suggest that atrial flutter induces reversible changes in sinus node function.

Aged↗

Large tip electrodes for successful elimination of atrial flutter resistant to conventional catheter ablation.

The most widely accepted criterion for successful radiofrequency catheter (RFC) ablation of typical atrial flutter is the development of bi-directional isthmus block. In a subset of patients, conventional RFC ablation fails to achieve this endpoint because deeper and wider lesions are required. We investigated the efficacy of a long 8-mm tip catheter in these cases. One hundred and seventy-four consecutive patients (137 male; 61 +/- 9 years) with recurrent typical atrial flutter underwent conventional RFC ablation first with a standard 4 mm tip catheter. In resistant cases (n = 52), ablation was continued using a large tip 8-mm catheter when the 4-mm tip catheter failed. Resistant atrial flutter was identified when 21 RFC pulses failed to reach the selected endpoint of bi-directional isthmus block or in cases of transient bi- directional block (at least 3 episodes). In 122 of the 174 patients (70%) conventional atrial flutter ablation was successfully performed with 13 +/- 5 RFC applications. In the remaining 52 subjects (30%), the ablation procedure was completed using the large tip electrode catheter. In 30 of these 52 patients (58%), the catheter was changed because of persistent intra-atrial conduction after 21 RFC pulses and in 22 (42%) because of intermittent conduction block after 11 +/- 5 applications. Using the large tip electrode catheter, the selected endpoint was achieved in all patients of both groups with 3 +/- 2 RFC pulses (power output of 50-60 W, pulse duration of 60 sec). No post-procedure complications were observed. After 15 +/- 5 months of follow-up, 16 patients (9%) had recurrence of atrial flutter. Five of the patients had been in the resistant group. In patients with atrial flutter resistant to conventional ablation therapy, the long tip (8-mm) catheter appears to be a safe and effective alternative to use of the conventional 4-mm tip catheter.

Atrial Flutter↗

Acute and long-term effects of consecutive radiofrequency applications on conduction properties of the subeustachian isthmus in type I atrial flutter.

INTRODUCTION: Bidirectional conduction block at the subeustachian isthmus predicts long-term efficacy of atrial flutter ablation. Limited data are available on the incidence and outcome of minor conduction changes such as unidirectional or incomplete block. This prospective study sought to systematically assess discrete acute and long-term alterations of bidirectional conduction prior to a complete conduction block. METHODS AND RESULTS: In 41 patients with type I atrial flutter, pulse propagation through the subeustachian isthmus during low lateral and proximal coronary sinus pacing was documented and analyzed following each consecutive radiofrequency (RF) application. In cases of altered conduction properties and noninducibility of atrial flutter, patients were followed-up for 12 months. Three sets of results were found. First, following RF application, 23 patients presented a progressive conduction delay prior to a complete conduction block. Second, RF application did not always affect counterclockwise and clockwise conduction simultaneously or to the same extent. In 13 patients, an initial alteration of counterclockwise conduction was present before an alteration of clockwise conduction; in 5 patients, clockwise conduction was primarily affected. Third, the recurrence rate of typical atrial flutter was 9% (2/22) in patients with a complete bidirectional conduction block, 54% (7/13) in patients with unidirectional conduction block, and 100% (6/6) in patients with sole bidirectional conduction delay. CONCLUSION: In 50% of the patients, consecutive RF applications resulted primarily in a progressive conduction delay rather than a sudden conduction block. Since counterclockwise and clockwise conduction were not always affected simultaneously or to the same extent, lateral as well as septal pacing is recommended for improvement of bidirectional conduction block. Normalization of primarily altered conduction and, therefore, recurrence of atrial flutter are high in all patients without bidirectional block.

Adult↗

Overdrive atrial pacing for conversion of atrial flutter: comparison of postoperative with nonpostoperative patients.

BACKGROUND: Previous studies have reported varying success rates in overdrive pace termination of atrial flutter. We hypothesized that these discrepancies might be caused by differences in study populations. Accordingly, we prospectively compared the success rate of pacing in patients with atrial flutter that occurred after heart surgery with that of patients with atrial flutter from other causes. METHODS AND RESULTS: The study population consisted of 65 consecutive patients referred for pace termination of typical (type I) atrial flutter. Pacing was performed in 30-second bursts, starting at the flutter cycle length, and repeated in 5-ms decrements until normal sinus rhythm or atrial fibrillation occurred. Normal sinus rhythm was restored in 38 (65%) patients. Of 20 patients whose flutter was precipitated by heart surgery, 19 (95%) were successfully pace terminated. In contrast, pace termination was successful in only 47% of the remainder of the population (P <.001). No other clinical parameters were predictive of outcome. CONCLUSIONS: We conclude that overdrive pacing is an effective means of terminating atrial flutter that has occurred after heart surgery. Alternative methods should be considered as the initial therapeutic approach in patients with atrial flutter from other causes.

Aged↗

Familial atrial standstill with coexistent atrial flutter.

A child with familial atrial standstill and a ventricular pacemaker had syncope due to atrial flutter that was treated by His-bundle ablation. Bradycardia protection alone may be insufficient in patients with atrial standstill.

Atrial Flutter↗

Atrial flutter secondary to hypokalemia.

Electrophysiologic studies support significant hypokalemia as a cause of atrial flutter in a patient without manifest heart disease. Atrial flutter, reproducibly initiated and terminated by rapid atrial pacing during hypokalemia, was not inducible after potassium correction. In an individual with existing atrial conduction disease, hypokalemia may generate both non-uniform atrial refractoriness and atrial premature beats, and it may facilitate the development of atrial flutter as a re-entrant arrhythmia.

Aged↗