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 577 records · Page 32Linked to original sources

Electrophysiologic studies in atrial flutter.

The clinical electrophysiologic approaches to atrial flutter (F) have been activation mapping and the observation of changes induced by programmed stimulation. Sequential endocardial activation mapping has recently yielded information indicating that common F is produced by a large right atrial (RA) reentry circuit, with counterclockwise rotation in the frontal plane, including the inferior vena cava in its center. Functional block in the crista terminalis and conduction slowing in the approaches to the atrioventricular node seem to be important to support reentry. F inscribing positive deflections in the inferior leads usually follows the same path, but in a clockwise direction. Atypical F may be produced by left atrial circuits. Atrial stimulation during F entrains the circuit, resetting it with each stimulus. Collision between antidromic and orthodromic activation during entrainment produces fusion that can be identified in the surface electrocardiogram. The last paced activation restarts F, unless circuit penetration has been enough to modify it by block or disorganization. Entrainment may result in F acceleration, with changes in activation sequence, suggesting a different type of reentry, possibly based on functional factors.

Atrial Flutter↗

Value of entrainment mapping in determining the isthmus-dependent nature of atrial flutter in the presence of amiodarone.

INTRODUCTION: Entrainment mapping is a useful procedure for localizing macroreentrant tachycardia circuits. In patients with isthmus-dependent atrial flutter, entrainment mapping from the isthmus during tachycardia results in postpacing intervals (PPI) close to the tachycardia cycle length (TCL). However, the influence of antiarrhythmic drugs on the method's value is not clearly established. The aim of our study was to assess the value of entrainment mapping in the presence of amiodarone in patients undergoing radiofrequency ablation (RFA) of isthmus-dependent atrial flutter. METHODS AND RESULTS: The study consisted of 83 patients with isthmus-dependent atrial flutter: 52 were taking amiodarone at the time of RFA (group 1) and 31 were in a drug-free state (group 2). Entrainment mapping was performed from the cavotricuspid isthmus, and PPI minus TCL was determined. The two groups had similar baseline clinical characteristics. In all patients, RFA of the isthmus resulted in termination of tachycardia, confirming the isthmus-dependent nature of the flutter. TCL was significantly longer in group 1 than in group 2 (263 +/- 31 msec vs 238 +/- 27 msec, P < 0.0002). PPI minus TCL at the isthmus was significantly longer in group 1 than in group 2 (17 +/- 17 msec vs 8 +/- 4 msec, P < 0.01). More patients in group 1 had PPI-TCL>20 msec compared to group 2 (37% vs 10%, P = 0.01). CONCLUSION: Amiodarone significantly alters the entrainment mapping response from the isthmus. In this setting, long return cycles exceeding the TCL by >20 msec do not exclude isthmus-dependent atrial flutter.

Aged↗

Progression of advanced interatrial block to atrial flutter: a prospectively-followed case.

Interatrial block (IAB; P wave > or = 110 ms), commonly associated with left atrial enlargement and its electromechanical dysfunction, is also a significant correlate of atrial tachyarrhythmias. While the arrhythmogenic mechanisms of atrial fibrillation and atrial flutter may indeed differ, there is actually considerably less literature showing evidence of prospective progression of IAB, be it partial or advanced, to atrial flutter. We present a unique case of atrial flutter occurring within months of diagnosis of advanced IAB in an otherwise healthy female to briefly generate our discussion on the possible reasons for this scenario.

Aged↗

Right atrial flutter due to lower loop reentry: mechanism and anatomic substrates.

BACKGROUND: The mechanisms of an atrial flutter (AFL) that is more rapid and at times more irregular than typical AFL are unknown. METHODS AND RESULTS: Twenty-nine patients with AFL were studied. Atrial electrograms were recorded from a 20-pole catheter placed against the tricuspid annulus (TA), with its distal electrodes lateral to the isthmus between the TA and the eustachian ridge (ER), and from the His bundle and coronary sinus catheters. Atrial extrastimuli were delivered in the TA-ER isthmus during typical AFL. Episodes of a right atrial flutter rhythm that was different from typical AFL were induced in 3 patients and occurred spontaneously in 3 patients. This sustained AFL, designated as lower-loop reentry (LLR), involved the lower right atrium (RA), as manifested by early breakthrough in the lower RA, wave-front collision in the high lateral RA or septum, and conduction through the TA-ER isthmus. Linear ablation resulting in bidirectional conduction block in the TA-ER isthmus terminated spontaneous LLR in 3 patients and rendered LLR noninducible in all patients. The cycle length of LLR was shorter than that of typical AFL (217+/-32 versus 272+/-40 ms, P<0. 01). Alternating LLR and typical AFL in 1 patient resulted in cycle length oscillation. CONCLUSIONS: LLR is a subtype of right atrial flutter and depends on conduction through the TA-ER isthmus.

Adult↗

Radiofrequency catheter ablation of common atrial flutter in 80 patients.

OBJECTIVES: The purpose of this study was to evaluate the efficacy and safety of radiofrequency catheter ablation of common atrial flutter and to determine the optimal target sites in a large series of patients. BACKGROUND: Recent studies report the efficacy of radiofrequency current application in the low right atrial region to interrupt and prevent recurrences of common atrial flutter. However, larger groups of patients are required to confirm the efficacy of this technique and to specify the target sites. METHODS: Two different approaches were used to target the ablation site in 80 consecutive patients. In the first 50 patients, target sites were localized using both anatomic landmarks and electrophysiologic variables. Three anatomic landmarks were used: area 1 = between the tricuspid valve and inferior vena cava orifice; area 2 = between the tricuspid valve and coronary sinus ostium; area 3 = between the inferior vena cava and coronary sinus. The electrophysiologic criterion was to ablate when there was a stable atrial electrogram during the plateau phase. In the next 30 patients we assessed the effect of application of radiofrequency energy in a single line in area 1, 2 or 3 in groups of 10 patients. RESULTS: Overall atrial flutter was interrupted and rendered noninducible after a single session in 72 patients (90%) and could not be interrupted in 8 (10%). The mean (+/- SD) number of radiofrequency applications was 12 +/- 8. After a mean (+/- SD) follow-up of 20 +/- 8 months, recurrences occurred in 14 patients (17%). The location of the final successful site in the first group of 50 patients was in area 1 in 39%, area 2 in 36% and area 3 in 25%. In the next 30 patients, when lines of radiofrequency lesions were placed at several sites, they produced success rates of 70%, 40% and 10% at areas 1, 2 and 3, respectively. CONCLUSIONS: Radiofrequency catheter ablation of atrial flutter can be performed with a high success rate and is safe. The highest success rate is achieved with radiofrequency energy applied in the isthmus between the inferior vena cava orifice and tricuspid valve.

Actuarial Analysis↗

Factors determining clockwise and counterclockwise conduction patterns in atrial reentrant tachycardias: a rabbit model of atrial flutter.

INTRODUCTION: In the development of atrial flutter due to reentry, the crista terminalis is supposed to pose a conduction barrier, but the role of its longitudinal conduction in determining the propagation pattern of the reentrant impulse is not known. In rabbit right atrial preparations, we induced reentrant atrial tachycardias and examined the effects of transverse section of the crista terminalis on the development and conduction patterns of arrhythmias. METHODS AND RESULTS: Right atrial preparations from 12 albino rabbits were placed endocardial surface down in a chamber with an array of 48 bipolar electrodes to draw activation maps. A single premature stimulus was delivered to induce tachycardias at the free wall. In the control, five instances of tachycardia per preparation were induced and another five were induced after cutting the crista terminalis. In the control, the mean duration of tachycardia was 127.1+/-25.2 seconds. The tachycardia was counterclockwise in 39 of 60 instances, clockwise in 12, and undetermined in 4 defined as "atypical." After transverse section of the crista terminalis, the duration was prolonged to 372.6+/-30.4 seconds, but the conduction patterns were not changed. In the free wall, counterclockwise reentry had a broader wavefront and faster conduction than clockwise reentry. CONCLUSION: Longitudinal conduction block at the crista terminalis contributed to maintenance of reentrant atrial tachycardias, but had no influence on their propagation patterns. Clockwise and counterclockwise rotation of impulses in reentrant tachycardias had different paths and velocities of the wavefront in the free wall of the right atrium.

Animals↗

Cardiac troponin T does not increase after electrical cardioversion for atrial fibrillation or atrial flutter.

OBJECTIVE: To determine whether cardiac troponin T increases after electrical cardioversion in patients with atrial fibrillation or atrial flutter. DESIGN: Serum creatine kinase (CK), creatine kinase-MB (CKMB), and cardiac troponin T were measured before, 24 hours, and 48 hours after cardioversion in 15 patients with atrial fibrillation or atrial flutter. RESULTS: 12 of the 15 patients (80%) were successfully cardioverted to sinus rhythm. The median number of shocks was three (range one to six), the median cumulative energy 710 J (50 to 1430 J), and the median peak energy 300 J (50 to 360 J). Total CK increased from a baseline median concentration of 92 (45 to 259) to 1324 (96 to 6660) U/l at 24 hours and 1529 (120 to 4774) U/l at 48 hours after cardioversion. There was a small increase in CKMB but the ratio of CKMB to CK did not increase. There was no increase in cardiac troponin T in any patient. CONCLUSIONS: Following electrical cardioversion of atrial fibrillation or atrial flutter, cardiac troponin T remains unchanged despite a large rise in total CK, indicating that the CK is derived from skeletal muscle and that myocardial injury does not occur. If cardiac troponin T is increased after cardioversion for atrial arrhythmias then other causes of myocardial damage should be sought.

Aged↗

Impact of the ECG for detection of intraatrial conduction block after atrial flutter ablation.

Induction of complete bidirectional conduction block via the posterior isthmus of the right atrium is introduced as a standard endpoint for catheter ablation of atrial flutter. The present study sought to investigate the impact of changes in P wave duration and morphology detected by the surface ECG during coronary sinus and posterolateral right atrial stimulation as a marker for conduction block. Morphology and duration changes of the paced P wave before and after radiofrequency catheter (RFC) ablation were estimated in 22 patients referred for ablation of atrial flutter. We looked for a morphology change of the terminal portion in the 12-lead ECG and an increment of P wave duration. In 16 of 22 patients in whom atrial flutter ablation resulted in a complete bidirectional block, the conduction block was unidirectional in 4 patients and conduction times remained unchanged in 2 patients. After induction of complete bidirectional block a change of the terminal portion of the P wave towards a more positive morphology in one or more inferior leads was detected in 14 (88%) of 16 patients during coronary sinus stimulation and in 15 (94%) of 16 patients during posterolateral right atrial stimulation. These changes were predominantly observed in the inferior leads. Positive morphology changes of the terminal P wave portion in the inferior leads indicating conduction block with a sensitivity of 86% and a specificity of 100% were observed. An increment of 10 ms or more in P wave duration indicates conduction block with a specificity of 100% and a sensitivity of 67%. There was a significantly larger increment of P wave duration during coronary sinus (CS) stimulation compared to posterolateral right atrial stimulation (38 +/- 21 vs 16 +/- 21 ms). The analysis of P wave duration and morphology in the inferior leads of the surface ECG is a reliable tool to assess the intraatrial conduction after atrial flutter ablation. Different conduction during coronary sinus and posterolateral right atrial pacing may cause a different P wave duration after ablation.

Aged↗

[Termination of atrial flutter using esophageal stimulation].

The risk of possible complications in atrial flutter leads to attempts to use all available therapeutic possibilities to eliminate this disorder of the cardiac rhythm. By oesophageal stimulation the sinus rhythm was restored in 40% and a change to atrial fibrillation was achieved in 50% of the patients. The advantages of this method include above all speed and the minimal risk of complications; the disadvantage of the method is the unpleasant sensation when the electrode is inserted and the painful perception of the stimuli. Oesophageal stimulation can be recommended as the method of choice in treatment of atrial flutter.

Atrial Flutter↗

[Atrial flutter: an update].

Invasive electrophysiologic studies have changed the clinical outlook for patients with atrial flutter. Recognition of the reentrant circuit responsible for typical atrial flutter has led to the development of catheter ablation techniques that can prevent recurrence in >90% of cases. In addition, general understanding of atrial tachycardias has changed radically, such that ECG-based classifications are now obsolete. Atypical reentrant circuits associated with surgical scars or fibrotic areas in either atrium, which are indistinguishable from focal tachycardias on ECG, have been identified. These circuits also seem amenable to treatment by ablation. Recently, a new type of reentrant tachycardia that could be problematic in the future has emerged in patients who have undergone extensive left atrial ablation for the treatment of atrial fibrillation. These atypical circuits can be characterized using the mapping and entrainment techniques initially developed for typical flutter. In these cases, electroanatomical mapping, involving the construction of a virtual anatomical model of the atria, is extremely helpful. Despite the success of ablation, long-term prognosis is frequently overshadowed by the appearance of atrial fibrillation, which suggests that flutter and fibrillation share a common arrhythmogenic origin that is not modified by cavotricuspid isthmus ablation. In contrast with our clear electrophysiologic understanding of atrial flutter, little is known about the natural history of the condition because the literature has traditionally grouped patients with flutter and fibrillation together. Consequently, the complex relationship between the two arrhythmias has still to be clearly delineated. Primary prevention and preventing the development of atrial fibrillation after ablation remain outstanding clinical challenges.

Anisotropy↗

[The effects of the ablation of atrial flutter in patients with and without a clinical history of paroxysmal atrial fibrillation].

BACKGROUND: Although the safety and effectiveness of radiofrequency (RF) transcatheter ablation in patients with atrial flutter (AFL) is well established, little attention is paid to previous history of associated paroxysmal atrial fibrillation (AF) and the recurrence of AFL after RF ablation. In addition, it is not known whether the elimination of AFL can modify the natural history of AF in patients who experience both of these arrhythmias. Accordingly, the aim of this study was to evaluate the effect of RF ablation of AFL in patients with or without a previous history of AF in terms of the incidence of both arrhythmias in the follow-up. METHODS: RF ablation of the atrial isthmus between tricuspid ring, coronary sinus os and inferior vena cava was performed in 27 patients (23 males, 4 females; mean age 61 +/- 9 years) according to the technique described by Cosio. Based on ECG pattern, twenty patients exhibited common or type 1 AFL (negative F waves in the inferior leads with a sawtooth morphology), while seven patients had both common and uncommon AFL (various surface F wave morphologies, generally positive F waves in the inferior leads). A history of association between AFL and paroxysmal AF was documented in 48% of patients, but AFL was the major arrhythmia. After ablation, the patients were followed up and the clinically documented occurrence of arrhythmias was determined. RESULTS: Based on clinical history before ablation, we compared patients with an association between AFL and AF (Gr AFL + AF; n = 13) vs patients with only AFL (Gr AFL; n = 14). The characteristics of the two groups were similar regarding age, sex, duration of symptom, structural heart disease, left atrial size, P-wave duration, AFL interruption during RF procedure, antiarrhythmic treatment before and after RF procedure, and duration of follow-up. During a follow-up of 12 +/- 6 months, AFL recurred in 10 patients (37%), 4 from Gr AFL + AF, and 6 from Gr AFL (p = NS). Episodes of paroxysmal AF occurred in 6 patients (22%), 5 from Gr AFL + AF and 1 from Gr AFL (p < 0.05). In Gr AFL + AF, the incidence of AF after ablation was significantly lower (1.8 +/- 0.6 vs. 0.7 +/- 1 episodes/year; p < 0.02). Characteristics of patients with or without AFL recurrence in the follow-up were similar. The percentage of patients with the occurrence of AFL or AF, associated or unassociated in the follow-up, was 55%. CONCLUSIONS: A history of paroxysmal AF before RF ablation of AFL is not predictive of long-term success or failure of the procedure when considering the recurrence of AFL alone. Nevertheless, the general results are disappointing because the majority of patients have arrhythmias, AFL or AF, associated or unassociated in the follow-up. A clinical history of AF before ablation is correlated with a higher incidence of AF in the follow-up. In any event, the incidence of AF episodes is lower in the follow-up, indicating a possible beneficial effect of AFL ablation on AF mechanisms.

Adult↗

Atrial tachycardia arising from the right atrial inferoseptum masquerading as common atrial flutter.

Radiofrequency catheter ablation was performed in 2 patients with atrial tachycardia (AT). In both cases the AT originated from the inferoseptal portion of the right atrium, and the cycle length was 210 ms. The surface ECG demonstrated common counterclockwise atrial flutter, probably caused by functional block in the clockwise direction at the cavo-tricuspid isthmus and posterior right atrium with rapid activation of the origin. Although rare (2%), AT originating from the inferoseptum of the right atrium should be considered when the surface ECG exhibits common atrial flutter.

Adult↗

Excitable gap composition in the presence of antiarrhythmic drugs in common human atrial flutter.

BACKGROUND AND OBJECTIVE: Recurrence of atrial flutter (AFl) on antiarrhythmic drugs is frequently observed. To determine the reasons for drug inefficacy, the electrophysiological parameters of AFl were studied in eight patients without drug, six patients on sotalol (Sot), eight patients on amiodarone (Amio) and four patients on propafenone (PPF) who presented to the electrophysiology laboratory for conversion of AFl by rapid atrial pacing. METHODS: A quadripolar electrode catheter was positioned in the right atrium in the pathway of the AFl circuit. The duration and composition of the excitable gap (EG) were determined by premature stimuli during AFl. RESULTS: The EG in AFl recurring on Sot (80 +/- 25 ms), Amio (78 +/- 13 ms) and PPF (83 +/- 26 ms) was not significantly different from that without drug (88 +/- 14 ms). Furthermore, a fully excitable portion of the EG was present whether with or without drug. CONCLUSIONS: AFl recurrence on Amio, PPF or Sot is associated with the continued presence of an EG and fully excitable portion. These findings explain the persistent viability of the AFl circuit despite drug therapy in these patients.

Adult↗

[Cardiac electrostimulation methods in the treatment, drug therapy selection and assessment of their antirelapse effect in atrial flutter].

Preliminary preparation of patients with atrial flutter (AF) using antiarrhythmic drugs permits enhancing efficiency of electrocardiostimulating method to arrest AF (up to 93.75%). The size of the amplitude F in transesophageal electrogramme (TEEG) and duration of the cycle of auricular contractions permit the results of the electrocardiostimulating arrest of AF to be predicted. AF of low amplitude wave F in TEEG turns, as a rule, to atrial fibrillation.

Adult↗

Cerebral thromboembolism after direct current cardioversion for pure atrial flutter.

The need for prophylactic anticoagulation before electrical cardioversion for atrial arrhythmias is clearly established in the case of atrial fibrillation. By contrast, such prophylaxis is not a current standard of care before cardioversion for pure atrial flutter, since this arrhythmia seems not to increase the risk of postcardioversion embolism. We present a patient who developed two cerebral embolisms 24 h after electrical cardioversion for pure atrial flutter. To our knowledge, this observation has not been previously reported.

Aged↗

Atrial flutter complicating neonatal Coxsackie B2 myocarditis.

A neonate presented with atrial flutter complicating acute Coxsackie B2 myocarditis. The tachyarrhythmia was successfully terminated with electrocardioversion followed by digoxin administration. The infant survived with no long-term cardiac sequelae. Atrial flutter is an unusual complication of Coxsackie myocarditis that has not previously been reported.

Atrial Flutter↗

Randomized comparison of anatomical versus voltage guided ablation of the cavotricuspid isthmus for atrial flutter.

OBJECTIVES: The purpose of this prospective study was to compare radiofrequency catheter ablation of the cavotricuspid isthmus using a strictly anatomic approach to an approach guided by a bipolar voltage map to avoid high voltage zones in the cavotricuspid isthmus. BACKGROUND: It is not clear whether local atrial electrogram amplitude influences the achievement of complete cavotricuspid isthmus block during radiofrequency catheter ablation for atrial flutter. METHODS: Thirty-two patients with atrial flutter were randomized to cavotricuspid isthmus ablation using an anatomical approach (group I, 16 patients) or guided by a bipolar voltage map (group II, 16 patients). A 3-dimensional electroanatomic mapping system and an 8-mm-tip ablation catheter were used in all patients. With the anatomical approach, an ablation line was created in the cavotricuspid isthmus at a 6 o'clock position in the 45 degree left anterior oblique projection. During voltage-guided ablation, a high-density bipolar voltage map of the cavotricuspid isthmus was created, and then contiguous applications of radiofrequency energy were delivered to create an ablation line through the cavotricuspid isthmus sites with the lowest bipolar voltage. RESULTS: Complete cavotricuspid isthmus conduction block was achieved in 100% of patients in each group. The mean maximum voltages along the line were 3.6 +/- 1.5 mV in group I, and 1.2 +/- 0.9 mV in group II (P < .01). Creating a high-density voltage map was associated with approximately 15-minute increase in the total procedure time (P = .2). During a mean follow-up of 177 +/- 40 days, there were no recurrences of atrial flutter in either group. There were no complications in either group. CONCLUSIONS: When cavotricuspid isthmus ablation for atrial flutter is performed with an 8-mm-tip catheter, complete block can be achieved in all patients regardless of local voltage. Ablation of high voltage zones is not associated with a higher recurrence rate. Therefore, anatomic ablation without voltage mapping is the preferred initial approach for cavotricuspid isthmus ablation.

Atrial Flutter↗

Intracardiac overdrive pacing as a treatment of atrial flutter in a horse.

A five-year-old warmblood mare with atrial fibrillation was treated with quinidine sulphate. The atrial rhythm changed to atrial flutter and, because there were toxic effects, the treatment was discontinued. Seven months after the occurrence of the atrial flutter, treatment with a rapid atrial pacing technique restored a normal sinus rhythm. One year after the pacing therapy the horse was still in sinus rhythm and had been brought back into training.

Animals↗