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 145 records · Page 8Linked to original sources
PubMed1990

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

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

Adult↗
PubMed2002

Atypical left atrial flutters.

Left atrial flutters are not as common as peri-tricuspidian circuits. Their systematic study is much more recent and had greatly benefited from the use of 3 D mapping systems. Reentry has been demonstrated as being the mechanism but the circuits are not stereotypical like in the right atrium. Multiple macroreentrant circuits with one or more loops have been described as well as small re-entrant circuits. The complexity and variability of these circuits is related to the presence of zone of block, slow conduction and electrically silent areas. They create the conditions for the arrhythmia maintenance as they stabilize the circuit and prevent short circuiting. Most of the patients with left atrial flutter have an underlying structural heart disease, but their arrhythmia is amenable to curative catheter ablation.

Atrial Flutter↗
PubMed2000

Efficacy and safety of oral dofetilide in converting to and maintaining sinus rhythm in patients with chronic atrial fibrillation or atrial flutter: the symptomatic atrial fibrillation investigative research on dofetilide (SAFIRE-D) study.

BACKGROUND: This double-blind, multicenter, placebo-controlled study determined the efficacy and safety of dofetilide in converting atrial fibrillation (AF) or atrial flutter (AFl) to sinus rhythm (SR) and maintaining SR for 1 year. METHODS AND RESULTS: Patients with AF or AFl (n=325) were randomized to 125, 250, or 500 microgram dofetilide or placebo twice daily. Dosages were adjusted for QTc response and, after 105 patients were enrolled, for calculated creatinine clearance (Cl(Cr)). Pharmacological cardioversion rates for 125, 250, and 500 microgram dofetilide were 6.1%, 9.8%, and 29.9%, respectively, versus 1.2% for placebo (250 and 500 microgram versus placebo; P=0.015 and P<0.001, respectively). Seventy percent of pharmacological cardioversions with dofetilide were achieved in 24 hours and 91% in 36 hours. For the 250 patients who successfully cardioverted pharmacologically or electrically, the probability of remaining in SR at 1 year was 0.40, 0.37, 0.58 for 125, 250, and 500 microgram dofetilide, respectively, and 0.25 for placebo (500 microgram versus placebo, P=0.001). Two cases of torsade de pointes occurred, 1 on day 2 and the other on day 3 (0.8% of all patients given active drug); 1 sudden cardiac death, classified as proarrhythmic, occurred on day 8 (0.4% of all patients given active drug). CONCLUSIONS: Dofetilide, a new class III antiarrhythmic agent, is moderately effective in cardioverting AF or AFl to SR and significantly effective in maintaining SR for 1 year. In-hospital initiation and dosage adjustment based on QTc and Cl(Cr) are necessary to minimize a small but nonnegligible proarrhythmic risk.

Administration, Oral↗
PubMed1999

Persistent atrial flutter in patients treated for atrial fibrillation with amiodarone and propafenone: electrophysiologic characteristics, radiofrequency catheter ablation, and risk prediction.

INTRODUCTION: Antiarrhythmic drugs have been reported to promote the conversion of atrial fibrillation to atrial flutter in patients with paroxysmal atrial fibrillation. However, information about the electrophysiologic mechanism and response to radiofrequency ablation of these drug-induced atrial flutters is limited. Furthermore, the determinants of the development of persistent atrial flutter in patients treated for atrial fibrillation with antiarrhythmic drugs are still unknown. METHODS AND RESULTS: Among the 136 patients treated for atrial fibrillation with amiodarone (n = 96) or propafenone (n = 40), 15 (11%, mean age 65.5 +/- 12.3 years) were identified to have subsequent development of persistent atrial flutter based on surface ECG characteristics during antiarrhythmic drug treatment. The mean interval between the beginning of drug treatment and the onset of atrial flutter was 5.0 +/- 5.5 months. Intracardiac mapping and entrainment studies revealed that 11 patients had counterclockwise typical atrial flutter, and 4 had clockwise typical atrial flutter. All 15 patients underwent successful ablation with creation of complete bidirectional isthmus conduction block. After a mean follow-up of 12.3 +/- 4.2 months, 14 (93%) of 15 patients who underwent successful ablation and continued taking antiarrhythmic drugs have remained in sinus rhythm. Univariate analysis of clinical variables demonstrated that only atrial enlargement was significantly related to the occurrence of persistent atrial flutter. CONCLUSION: In patients with atrial fibrillation, persistent typical atrial flutter might occur during antiarrhythmic drug treatment, and atrial enlargement was a risk factor for the development of such an arrhythmia. Radiofrequency ablation and continuation of pharmacologic therapy offered a safe and effective means of achieving and maintaining sinus rhythm.

Aged↗
PubMed2001

Classification of atrial flutter and regular atrial tachycardia according to electrophysiologic mechanism and anatomic bases: a statement from a joint expert group from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology.

Regular atrial tachycardias classically are classified into flutter or tachycardia, depending on the rate and presence of a stable baseline on the ECG. However, current understanding of electrophysiology atrial tachycardias makes this classification obsolete, because it does not correlate with mechanisms. The proposed classification is based on electrophysiologic mechanisms, defined by mapping and entrainment. Radiofrequency ablation of a critical focus or isthmus can afford proof. Focal tachycardias are characterized by radial spread of activation and endocardial activation not covering the whole cycle. Ablation of the focus of origin interrupts the tachycardia. The mechanism of focal firing is difficult to ascertain by clinical methods. Macroreentrant tachycardias are characterized by circular patterns of activation that cover the whole cycle. Fusion can be shown during entrainment on the ECG or by multiple endocardial recordings. Ablation of a critical isthmus interrupts the tachycardia. Macroreentry can occur around normal structures (terminal crest, eustachian ridge) or around atrial lesions. The anatomic bases of these tachycardias must be defined, to guide appropriate treatment. Atrial flutter is a mere description of continuous undulation on the ECG, and only some strictly defined typical flutter patterns correlate with right atrial macroreentry bounded by the tricuspid valve, terminal crest, and caval vein orifices. This classification should be considered open, as some classically described tachycardias, such as reentrant sinus tachycardia, inappropriate sinus tachycardia, and type II atrial flutter, cannot be classified accurately. Furthermore, the possibility of fibrillatory conduction makes the limits with atrial fibrillation still ill defined.

Animals↗
PubMed2003

Atrial electrogram amplitude and efficacy of cavotricuspid isthmus ablation for atrial flutter.

Large atrial electrogram amplitudes recorded in the cavotricuspid isthmus (CTI) may reflect thick atrial musculature. For this reason, in patients with atrial flutter, the efficacy of an application of conventional radiofrequency energy may be related to the amplitude of the local atrial electrogram. In 100 consecutive patients (mean age 59 +/- 13 years) with atrial flutter, contiguous applications of radiofrequency energy were delivered in the CTI. The criterion for complete CTI block was the presence of widely split double potentials (>110 ms) along the entire ablation line during pacing from the coronary sinus and posterolateral right atrium. The atrial electrogram amplitude was measured before and after applications of radiofrequency energy at sites of gaps in the ablation line. Complete CTI block was achieved in 90 (90%) of the 100 patients. The mean atrial electrogram amplitudes at gap sites where an application of radiofrequency energy did and did not result in complete block were 0.36 +/- 0.42 and 0.67 +/- 0.62 mV, respectively (P < 0.01). The positive and negative predictive values (for complete block) of a >/=50% decrease in electrogram amplitude after an application of radiofrequency energy were 100% and 35%, respectively. The mean atrial electrogram amplitude is larger at CTI sites where complete isthmus block cannot be achieved with conventional radiofrequency energy. The efficacy of conventional radiofrequency ablation may be improved by identifying areas in the CTI where the voltage is relatively low.

Atrial Flutter↗
PubMed1992

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

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

Action Potentials↗
PubMed1996

Atrial flutter mapping and ablation II. Radiofrequency ablation of atrial flutter circuits.

The definition of the anatomical substrate of reentry in atrial flutter has allowed the recognition of narrow, critical areas of the circuit, where radiofrequency ablation can interrupt reentry. In common flutter the isthmus between the inferior vena cava and the tricuspid valve appears the best target, but ablation between the coronary sinus and tricuspid valve can also be effective in some cases. In atypical flutter using the same circuit as common flutter in a "clockwise" direction, ablation of the same isthmus is effective. Flutter interruption is the main objective, but it does not mean complete isthmus ablation. If flutter remains inducible, new applications are delivered in the isthmus, until it is made noninducible. Complications are rare. Despite attaining noninducibility, flutter may recur, and new procedures may be needed to prevent recurrence. Atrial fibrillation can occur in up to 30% of the cases during follow-up, but it is generally well controlled with antiarrhythmic drugs, that were ineffective to treat flutter before ablation. In reentry circuits based on surgical atrial scars, ablation of an isthmus between the scar and the inferior vena cava can also be effective. Left atrial circuits are not known well enough to guide successful ablation.

Animals↗
PubMed2000

Atypical atrial flutter originating in the right atrial free wall.

BACKGROUND: Data from experimental models of atrial flutter indicate that macro-reentrant circuits may be confined by anatomic and functional barriers remote from the tricuspid annulus-eustachian ridge atrial isthmus. Data characterizing the various forms of atypical atrial flutter in humans are limited. METHODS AND RESULTS: In 6 of 160 consecutive patients referred for ablation of counterclockwise and/or clockwise typical atrial flutter, an additional atypical atrial flutter was mapped to the right atrial free wall. Five patients had no prior cardiac surgery. Incisional atrial tachycardia was excluded in the remaining patient. High-density electroanatomic maps of the reentrant circuit were obtained in 3 patients. Radiofrequency energy application from a discrete midlateral right atrial central line of conduction block to the inferior vena cava terminated and prevented the reinduction of atypical atrial flutter in each patient. Atrial flutter has not recurred in any patient (follow-up, 18+/-17 months; range, 3 to 40 months). CONCLUSIONS: Atrial flutter can arise in the right atrial free wall. This form of atypical atrial flutter could account for spontaneous or inducible atrial flutter observed in patients referred for ablation and is eliminated with linear ablation directed at the inferolateral right atrium.

Aged↗
PubMed1991

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

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

Action Potentials↗
PubMed1997

Left atrial appendage "stunning" after electrical cardioversion of atrial flutter: an attenuated response compared with atrial fibrillation as the mechanism for lower susceptibility to thromboembolic events.

OBJECTIVES: This study sought to determine whether left atrial appendage stunning occurs in patients with atrial flutter and to compare left atrial appendage function in the pericardioversion period with that in patients with atrial fibrillation. BACKGROUND: Left atrial appendage stunning has recently been proposed as a key mechanistic phenomenon in the etiology of postcardioversion thromboembolic events in atrial fibrillation. Atrial flutter is thought to be associated with a negligible risk of thromboembolic events; therefore, anticoagulation is commonly withheld before and after cardioversion in these patients. METHODS: Sixty-three patients with atrial flutter (n = 19) or atrial fibrillation (n = 44) underwent transesophageal echocardiography immediately before and after electrical cardioversion. In addition to assessing the presence of thrombus and spontaneous echo contrast, we measured left atrial appendage emptying velocity and calculated shear rates by pulsed wave Doppler and two-dimensional echocardiography. RESULTS: Patients with atrial flutter exhibited greater left atrial appendage flow velocities before cardioversion than those with atrial fibrillation (42 +/- 19 vs. 28 +/- 15 cm/s [mean +/- SD], p < 0.001). Left atrial appendage shear rates were also higher in patients with atrial flutter (103 +/- 82 vs. 59 +/- 37 s-1, p < 0.001). After cardioversion, left atrial appendage flow velocities decreased compared with precardioversion values in patients with atrial fibrillation (28 +/- 15 before to 15 +/- 14 cm/s after cardioversion, p < 0.001) and atrial flutter (42 +/- 19 to 27 +/- 18 cm/s, respectively, p < 0.001). Shear rates decreased from 59 +/- 37 before cardioversion to 30 +/- 31 s-1 after cardioversion in atrial fibrillation (p < 0.001), and from 103 +/- 82 s to 65 +/- 52 s-1, respectively (p < 0.001), in atrial flutter. This decrease in flow velocity from before to after cardioversion occurred in 36 (82%) of 44 patients with atrial fibrillation and 14 (74%) of 19 with atrial flutter. The impaired left atrial appendage function after cardioversion was less pronounced in the group with atrial flutter (27 +/- 18 cm/s for atrial flutter vs. 15 +/- 14 cm/s for atrial fibrillation, p < 0.001). New or increased spontaneous echo contrast occurred in 22 (50%) of 44 patients with atrial fibrillation versus 4 (21%) of 19 with atrial flutter (p < 0.05). CONCLUSIONS: Left atrial appendage stunning also occurs in patients with atrial flutter, although to a lesser degree than in those with atrial fibrillation. These data suggest that patients with atrial flutter are at risk for thromboembolic events after cardioversion, although this risk is most likely lower than that in patients with atrial fibrillation because of better preserved left atrial appendage function.

Aged↗
PubMed1977

High reversion of atrial flutter to sinus rhythm after atrial pacing in patients with pulmonary disease.

The effect of atrial pacing on atrial flutter was evaluated in 36 consecutive episodes in 33 patients. Seventeen episodes occurred in a pulmonary setting, 14 of these in patients with chronic pulmonary disease. Twenty-four (67 percent) of the 36 episodes converted to sinus rhythm within one minute after atrial pacing. In nine (25 percent) of the 36 episodes, atrial fibrillation developed after atrial pacing. Atrial flutter was not affected by atrial pacing in three (8 percent) of the 36 episodes.n 12 (86 percent) of the 14 patients with chronic pulmonary disease and in 14 (82 percent) of the 17 patients in whom a pulmonary setting was responsible for atrial flutter, atrial pacing caused conversion to sinus rhythm. Atrial pacing may be the treatment of choice for atrial flutter in patients with pulmonary disease because of its excellent rate of success in this subgroup whose risk of cardioversion is increased by poor anesthetic tolerance and hypoxia.

Aged↗
PubMed2001

Electrogram polarity and cavotricuspid isthmus block during ablation of typical atrial flutter.

INTRODUCTION: The atrial activation sequence around the tricuspid annulus has been used to assess whether complete block has been achieved across the cavotricuspid isthmus during radiofrequency ablation of typical atrial flutter. However, sometimes the atrial activation sequence does not clearly establish the presence or absence of complete block. The purpose of this study was to determine whether a change in the polarity of atrial electrograms recorded near the ablation line is an accurate indicator of complete isthmus block. METHODS AND RESULTS: Radiofrequency ablation was performed in 34 men and 10 women (age 60 +/- 13 years [mean +/- SD]) with isthmus-dependent, counterclockwise atrial flutter. Electrograms were recorded around the tricuspid annulus using a duodecapolar halo catheter. Electrograms recorded from two distal electrode pairs (E1 and E2) positioned just anterior to the ablation line were analyzed during atrial flutter and during coronary sinus pacing, before and after ablation. Complete isthmus block was verified by the presence of widely split double electrograms along the entire ablation line. Complete bidirectional isthmus block was achieved in 39 (89%) of 44 patients. Before ablation, the initial polarity of E1 and E2 was predominantly negative during atrial flutter and predominantly positive during coronary sinus pacing. During incomplete isthmus block, the electrogram polarity became reversed either only at E2, or at neither E1 nor E2. In every patient, the polarity of E1 and E2 became negative during coronary sinus pacing only after complete isthmus block was achieved. In 4 patients (10%), the atrial activation sequence recorded with the halo catheter was consistent with complete isthmus block, but the presence of incomplete block was accurately detected by inspection of the polarity of E1 and E2. CONCLUSION: Reversal of polarity in bipolar electrograms recorded just anterior to the line of isthmus block during coronary sinus pacing after ablation of atrial flutter is a simple, quick, and accurate indicator of complete isthmus block.

Adult↗
PubMed1998

Electrical-anatomic correlations between typical atrial flutter and intra-atrial re-entry following atrial surgery.

It is well known that in typical (or type I) atrial flutter, conduction proceeds counterclockwise, up the interatrial septum and down the right atrial wall anterior to the crista terminalis (CT). Recent careful mapping studies using entrainment pacing have clearly shown the importance of the CT and the eustachian valve ridge (EVR), which act as fixed barriers to intra-atrial conduction and interact with other barriers, including the tricuspid valve, inferior vena cava (IVC), and coronary sinus os, to create a long macroreentrant circuit. Ablative lesions are directed at the isthmus between the tricuspid valve and the IVC or between the tricuspid valve and the EVR. Patients who have had cardiac surgery may have typical atrial flutter, either counterclockwise or clockwise, and prior surgery may act to stabilize the circuit. Such patients may also have atypical flutter, which does not utilize this circuit. Surgical closure of septal defects requires a long anterior oblique atriotomy. Commonly, reentrant circuits are identified that use this barrier, as well as the tricuspid valve and CT, and are confined to the anterior atrial wall and do not involve the typical flutter isthmus. These may be ablated at the lower or the upper end of the atriotomy, extending the block to the tricuspid valve, IVC, or superior vena cava. After the Senning or Mustard procedure, typical flutter is common, and the baffle bisects the isthmus at the site of the EVR, perhaps enforcing block. Anterior atriotomy-mediated reentry also is seen, and both circuits need to be approached in a retrograde manner. After the Fontan atriopulmonary connection, atriotomies and atrial dilation may interact to make reentry more likely. After the "lateral tunnel" Fontan (cavopulmonary connection) suture lines are similar to those of the Senning procedure, but nearly all right atrial anatomy is in the pulmonary venous atrium. Such circuits may need to be approached via an atrial fenestration.

Adult↗
PubMed1976

[Atrial flutter with an audible atrial sound (author's transl)].

In a case of rheumatic valve disease atrial sounds could be heard and recorded on the phonocardiogram during atrial flutter at a rate of 260/min and an atrioventricular block of 3:1 and 5:1. The atrial flutter sounds were also recorded in the apex-cardiogram and as a slight but rapid motion of the anterior mitral valve leaflet in the echocardiogram. These atrial sounds were recorded both in systole and diastole and disappeared after cardiac failure had been treated and sinus rhythm restored. This case and 19 others reported in the medical literature indicate that for atrial sounds to become audible requires high-grade atrioventricular block and increased atrial contractions with increased ventricular filling. The sounds have been proven to originate in the atrium, the characteristics of the sound being similar to those of an opening snap.

Atrial Flutter↗
PubMed2001

Coexistence of type I atrial flutter and intra-atrial re-entrant tachycardia in patients with surgically corrected congenital heart disease.

OBJECTIVES: This study assessed the coexistence of intra-atrial re-entrant tachycardia (IART) and isthmus-dependent atrial flutter (IDAF) in patients presenting with supraventricular tachyarrhythmias after surgical correction of congenital heart disease (CHD). BACKGROUND: In patients with CHD, atrial tachyarrhythmias may result from IART or IDAF. The frequency with which IART and IDAF coexist is not well defined. METHODS: Both IDAF and IART were diagnosed in 16 consecutive patients using standard criteria and entrainment mapping. Seven patients had classic atrial flutter morphology on surface electrocardiogram (ECG), whereas nine had atypical morphology. RESULTS: A total of 24 circuits were identified. Three patients had IDAF only, five had IART only, seven had both, and one had a low right atrial wall tachycardia that could not be entrained. Twenty-two different reentry circuits were ablated. Successful ablation was accomplished in 13 of 14 (93%) IART and 9 of 10 (90%) IDAF circuits. There was one IART recurrence. The slow conduction zone involved the region of the right atriotomy scar in 12 of 14 (86%) IART circuits. No procedural complications and no further recurrences were seen after a mean follow-up of 24 months. CONCLUSIONS: Both IDAF and IART are the most common mechanisms of atrial re-entrant tachyarrhythmias in patients with surgically corrected CHD, and they frequently coexist. The surface ECG is a poor tool for identifying patients with coexistent arrhythmias. The majority of IART circuits involve the lateral right atrium and may be successfully ablated by creating a lesion extending to the inferior vena cava.

Adolescent↗
PubMed1990

Atrial endocardial mapping in the rare form of atrial flutter.

Endocardial atrial activation mapping was performed in 7 patients with rare atrial flutter (AF), inscribing predominantly positive deflections on leads II, III and aVF. In 2 cases both a rare and a common AF were mapped on different occasions. Every case displayed circular right atrial activation. In 5 of the 7 cases rare AF direction was clockwise (craniocaudal in the septum and posterior wall and caudocranial on the lateral and anterior walls). In 2 cases rare AF direction was counterclockwise (caudocranial in the septum and posterior wall and craniocaudal in the lateral and anterior walls). Both common AF rotated counterclockwise. A "line" of conduction delay or block was present in both clockwise and counterclockwise circuits between the posterior and lateral walls, in the probable location of the crista terminalis. This line of block extended the central obstacle made by the inferior vena cava toward, but perhaps not all the way to, the superior vena cava, making activation rotate roughly around the tricuspid ring. The ridge between the inferior vena cava and the tricuspid ring was a critical anatomic "closing" point in all clockwise and counterclockwise circuits. Right atrial macroreentry underlies rare AF. Direction of activation tends to be opposite to that in common AF. The cause of the positive deflection is unclear.

Adult↗
PubMed2000

Electrical remodeling of the atria associated with paroxysmal and chronic atrial flutter.

BACKGROUND: Atrial electrical remodeling may be important for the initiation and perpetuation of atrial arrhythmias. Whether paroxysmal atrial flutter (AFL) and chronic AFL cause electrical remodeling of the atria has not been conclusively determined. METHODS AND RESULTS: Before radiofrequency ablation of paroxysmal AFL, 15 patients in sinus rhythm were evaluated under autonomic blockade. Lateral right atrial (LRA) effective refractory periods (ERPs) at 600 and 450 ms were measured before and at 1-minute intervals for 10 minutes after spontaneous or pace termination of a 5- to 10-minute period of induced AFL. In 10 patients with chronic AFL, LRA, septal, and coronary sinus (CS) ERPs and corrected sinus node recovery times (cSNRTs) at 600 and 450 ms were measured under autonomic blockade 15 minutes, 30 minutes, and 3 weeks after termination of chronic AFL by ablation. In the paroxysmal AFL group, LRA ERPs decreased by 18% at 600 ms and 12% at 450 ms (P:<0.01) after induced AFL and recovered to baseline over approximately 5 minutes. Atrial fibrillation developed during AFL in 3 patients and during ERP testing in 3 patients when refractoriness was at its nadir. In the chronic AFL group, LRA, septal, and CS ERPs at 3 weeks were significantly greater than at 15 and 30 minutes after termination of chronic AFL at both cycle lengths (P:<0.01). Three weeks after ablation, cSNRT decreased 35% at 600 ms (P:<0.05) and decreased 44% at 450 ms (P:<0. 05). Both ERPs and cSNRTs measured 15 and 30 minutes after ablation of chronic AFL were not significantly different. CONCLUSIONS: Both paroxysmal AFL and chronic AFL cause reversible electrical remodeling of the atria but demonstrate different time courses of recovery.

Aged↗