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A unified functional/anatomic substrate for circus movement atrial flutter: activation and refractory patterns in the canine right atrial enlargement model.

OBJECTIVES: This study was designed to test the concept of a functional/anatomic interaction in a canine model of reentry based on right atrial enlargement and to elucidate the electrophysiologic basis for functional conduction block. BACKGROUND: The monotonic feature of atrial flutter suggests a uniform substrate for the arrhythmia. Atrial flutter in the sterile pericarditis model is due to single-loop circus movement around a functional or a functional/anatomic obstacle near the atrioventricular (AV) ring. Sustained circus movement requires a critical interaction of a functional arc of block, a natural obstacle, the AV ring and a zone of slow conduction. The location of the inferior vena cava predisposes the lower right atrium to single-loop reentry. METHODS: In 11 dogs with right atrial enlargement, 127 bipolar epicardial electrograms were obtained during atrial flutter. For correlation of activation and refractory maps, the effective refractory period under each electrode was determined using the extrastimulus technique. RESULTS: Atrial flutter was due to single-loop reentry around functional arcs of block near the AV ring (n = 2) or around functional/anatomic obstacles (n = 8) involving the inferior vena cava. A slow zone was located between the arc and the AV ring and between the inferior vena cava and AV ring, respectively. During initiation, the arc joined the AV ring, forcing activation to proceed around the free end of the arc before breaking through the arc near the AV ring. Arrhythmia termination required the arc of block to rejoin the AV ring. Inducibility of sustained atrial flutter was associated with a marked spatial dispersion of refractoriness. The configuration of the functional arc of block was critically dependent on the spatial pattern of refractoriness. CONCLUSIONS: Atrial flutter requires a similar functional or functional/anatomic substrate independent of the underlying etiology. The spatial distribution of refractoriness in enlarged canine atria provides an adequate substrate for the development of functional conduction block.

Animals↗

Prevalence, pathophysiology, and clinical significance of post-heart transplant atrial fibrillation and atrial flutter.

BACKGROUND: Atrial rhythm disturbances, in particular atrial fibrillation (AF) and flutter (AFL), are common in the denervated transplanted heart. However, there is a relative paucity of data in the prevalence, mechanism of arrhythmia, and long-term significance. OBJECTIVES: (1) Determine the prevalence of AF and AFL in heart transplant patients, (2) define the echo/Doppler features associated with arrhythmia, and (3) evaluate the impact of arrhythmia on long-term survival. METHODS: All patients who received an orthotopic heart transplant at the Mayo Clinic, Rochester, Minnesota, between 1988 and 2000 were included. Analysis of serial electrocardiograms and Holter monitor records provided evidence of AF or AFL development. Variables including general patient demographics, histology-proven rejection numbers and grades, results of serial coronary angiography, endomyocardial biopsy specimens, and echocardiographic studies performed at 6 weeks and 3 years after transplant were obtained to determine variables predictive of arrhythmia development. RESULTS: There were 167 heart transplant recipients, of which 16 (9.5%) developed AF and another 25 (15.0%) developed AFL over 6.5 +/- 3.4 years. Patients who developed AF or AFL had lower left ventricular (LV) ejection fractions (56.6% +/- 1.6% vs 62.5% +/- 1.5%, p < 0.05), higher LV end-systolic dimensions (LVESD) (33.6 +/- 1.12 mm vs 29.7 +/- 0.97 mm, p < 0.01), higher right atrial volume indexes (43.2 +/- 12.3 ml vs 35 +/- 5.3 ml, p < 0.03), lower mitral deceleration time (145 +/- 8 msec vs 160 +/- 12 msec, p < 0.05), and lower late mitral annulus tissue a' velocities (0.06 +/- 0.005 cm/sec vs 0.08 +/- 0.01 cm/sec, p < 0.02) compared with an age- and gender-matched Sinus Rhythm Group. Grade 3 rejection was a time-dependent covariate predictor of AFL risk (hazard ratio [HR], 2.95; 95% confidence interval [CI], 1.3-6.6, p < 0.008) but not AF (HR, 2.264; 95% CI, 0.72-7.1; p = 0.10). Thirty-nine of 167 patients died: 13 in the arrhythmia group and 26 in the normal sinus rhythm group. Development of atrial dysrhythmia adversely affected the outcome in the first 5 years (p < 0.001) compared with normal sinus rhythm. Predictors of long-term mortality included AF/AFL (HR, 2.88; 95% CI, 1.38-5.96; p < 0.004), age at transplant (HR, 1.04; 95% CI, 1.00-1.07, p < 0.03), coronary artery disease (HR, 2.655; 95% CI, 1.25-5.64; p = 0.01), pre-transplant cardiac amyloidosis (HR, 5.02; 95% CI 2.37-10.62; p < 0.001), right atrial volume index (HR, 1.03; 95% CI, 1.00-10.7; p = 0.03), mitral deceleration time <160 msec (p < 0.01), and LVESD >30 mm (p < 0.04). CONCLUSION: Development of AF/AFL post-heart transplantation is not uncommon and is associated with decreased long-term survival. Cumulative effects of repeated moderate-to-severe (grade 3 or more) rejections that result in increased cardiac fibrosis are associated with the development of AFL, but not AF. Similarly advanced restrictive diastolic dysfunction caused by fibrosis from repeated moderate-to-severe (grade 3 or more) rejections was predominant in the patients with arrhythmia and was a marker of poor long-term outcome.

Adult↗

The natural history of lone atrial flutter.

BACKGROUND: The natural history of atrial flutter is not well defined. OBJECTIVE: To report the risk for stroke, conversion to atrial fibrillation, and anticoagulation for lone atrial flutter. DESIGN: Retrospective cohort analysis. SETTING: A clinically based longitudinal study of inpatients and outpatients with atrial flutter. PATIENTS: The authors compared the stroke rate in 59 patients with atrial flutter with rates in a sample in which age- and sex-specific ischemic cerebrovascular event rates were determined and in a sample of nonhypertensive patients with lone atrial fibrillation. The risk for developing atrial fibrillation after presenting with atrial flutter is also reported. MEASUREMENTS: Electrocardiograms and clinical data were collected and reviewed for each study participant. RESULTS: After adjustment for age and sex, patients with atrial flutter had a higher incidence of thromboembolic events than the sample control patients and patients with atrial fibrillation. Atrial fibrillation developed in 56% of patients with atrial flutter. CONCLUSIONS: Lone atrial flutter has a stroke risk at least as high as lone atrial fibrillation and carries a higher risk for subsequent development of atrial fibrillation than in the general population. Anticoagulation should be considered for all patients with atrial flutter who are older than 65 years of age.

Adult↗

Combined amiodarone and silymarin treatment, but not amiodarone alone, prevents sustained atrial flutter in dogs.

UNLABELLED: Amiodarone/Silymarin Treatment for Sustained Atrial Flutter. INTRODUCTION: Because amiodarone generates free radicals that may mediate amiodarone's toxicity, simultaneous therapy with an antioxidant might be beneficial if the antioxidant did not impair amiodarone's antiarrhythmic action. We tested whether simultaneous administration of a flavonoid antioxidant, silymarin, altered the electrophysiologic (EP) actions of amiodarone in 62 open chest dogs with electrically induced atrial flutter created by a Y-shaped right atrial incision. METHODS AND RESULTS: Fifteen dogs received oral amiodarone (600 mg/day); 15 dogs received amiodarone (600 mg/day) and silymarin (70 mg bid); and 8 dogs received silymarin (70 mg bid) alone. All dosing was for 8 weeks; 24 control dogs received no drugs prior to induction of atrial flutter. Atrial flutter was induced by rapid right atrial pacing, and EP measurements were made before (presurgical) and after (postsurgical) creation of a Y-shaped right atrial incision. There was no difference in the frequency of induction of atrial flutter lasting >30 minutes among amiodarone-treated (8/15 [53%]), silymarin-treated (4/6 [67%]), and control (15/21 [71%]) groups, whereas the frequency of induction in the amiodarone+silymarin dogs (2/15 [13%]) was significantly reduced (P = 0.008) compared with the other three groups. Both amiodarone and amiodarone+silymarin treatment prolonged the presurgical and postsurgical right atrial effective refractory period (P = 0.012) compared with control; however, there was no significant difference in either parameter between the amiodarone+silymarin-treated and amiodarone-treated groups. The increase in atrial flutter mean cycle length (postsurgical minus presurgical) was significantly (P = 0.005) less in the amiodarone+silymarin-treated and control dogs compared with the amiodarone-treated dogs (16 +/- 11 msec for amiodarone+silymarin; 24 +/- 8 msec for control; and 42 +/- 14 msec for amiodarone treatment). Amiodarone+silymarin treatment resulted in a longer postsurgical right atrial refractory period (155 +/- 13 msec) than atrial flutter mean cycle length (154 +/- 19 msec), consistent with reduction and/or elimination of the excitable gap. Silymarin alone did not exert significant EP or antiarrhythmic action. CONCLUSION: Amiodarone exerted no preventative antiarrhythmic action in this atrial flutter model, probably because it could not reduce the excitable gap of atrial flutter. However, an antioxidant, silymarin, without a direct antiarrhythmic action, when administered together with amiodarone, potentiated amiodarone's antiarrhythmic actions and prevented sustained atrial flutter by reduction and/or elimination of the excitable gap.

Amiodarone↗

Polycardiographic study of atrial flutter.

The modifications that atrial flutter determines on the phonocardiogram, apexcardiogram, carotid pulse tracing, jugular venous pulse tracing, and indirect (esophageal) left atrial pulse tracing were studied. On the basis of the data here presented and that of the literature, a polygraphic profile of atrial flutter has been constructed as follows: notable variability of the intensity and of the richness of the vibratory components of the first and second heart sound; regularly alternating intervals between successive atrial sounds, each one of which consists of two groups of vibrations; deformations of all mechanographic tracings corresponding with "F" waves of the ECG. The interpretation of various polygraphic reports contributes to the understanding of the physiopathogenesis of atrial flutter.

Adult↗

Lower loop reentry as a mechanism of clockwise right atrial flutter.

BACKGROUND: Right atrial reentrant tachycardia resulting from lower loop reentry (LLR) around the inferior vena cava (IVC) has been described recently. However, all reported cases of LLR in the literature have negative flutter waves on the inferior surface ECG leads similar to that of counterclockwise typical atrial flutter around the tricuspid annulus (TA). Right atrial flutter with positive flutter waves in the inferior ECG leads has been assumed to rotate as a single reentrant activation wave front around the TA, and the role of LLR in those patients is not known. METHODS AND RESULTS: Twelve consecutive patients with flutter wave morphology on surface ECG consistent with clockwise atrial flutter were studied. The endocardial activation pattern recorded from conventional multipolar electrode catheters was characteristic of clockwise atrial flutter around the TA. Entrainment pacing in all 12 patients and 3D activation sequence mapping in 7 patients, however, revealed clockwise LLR involving the lower right atrium around the IVC in 7 patients, figure-of-8 double-loop reentry around both the IVC and TA in 4, and single reentrant loop around the TA in 1. Linear radiofrequency ablation in the isthmus between the TA and IVC (TI isthmus) terminated the tachycardia in all patients. CONCLUSIONS: Surface ECG flutter wave morphology and limited recording intracardiac sites proved insufficient to delineate the precise mechanism of the TI isthmus-dependent clockwise right atrial flutters. Most right atrial flutters with positive flutter wave on surface ECG may be supported by a reentrant circuit around the IVC or a figure-of-8 double-loop reentry involving both the IVC and TA.

Aged↗

Alternans of atrial action potentials during atrial flutter as a precursor to atrial fibrillation.

BACKGROUND: The mechanisms underlying the transition of typical atrial flutter (Afl) to fibrillation (AF) remain unclear. We set out to test the hypothesis that Afl disorganizes to AF via alternans of atrial action potentials. METHODS AND RESULTS: In 38 patients with Afl, monophasic action potentials (MAPs) were recorded at the isthmus and either high or low right atrium (HRA, LRA) during overdrive pacing to 160 ms or to the initiation of AF, whichever came first. MAP duration measured at 90% repolarization was longer at the isthmus in all patients, and failed to shorten with rate, compared with the HRA (n=38) or LRA (n=5). In 20 patients who developed AF, progressive pacing first caused alternans of isthmus MAP duration and amplitude at mean cycle length of 219+/-45 ms, followed by AF at a mean onset cycle length of 184+/-38 ms. Subsets of this group showed spontaneous action potential duration alternans at the isthmus (11 of 20 patients) and 2:1 isthmus conduction block immediately preceding AF (4 of 20 patients). In the 18 patients who did not develop AF, MAP alternans was less common (9 of 18 patients; P<0.0003), and occurred only at faster pacing (cycle length=169+/-25 ms; P<0.05). CONCLUSIONS: In patients with typical Afl, action potential duration rate maladaptation at the isthmus may lead to action potential duration alternans and conduction block preceding the transition to AF. These isthmus characteristics may enable the spontaneous initiation of AF through wavefront fractionation and may explain the benefits of isthmus ablation in preventing AF recurrence.

Action Potentials↗

Simultaneous surgical treatment of atrial septal defect and atrial flutter using a simple modification of the atrial incision.

The reentrant circuit of common atrial flutter is known to be located in the right atrium between two anatomical barriers. Recent electrophysiologic studies have defined the tricuspid annulus as the anterior barrier, and the terminal crest and its continuation as the eustachian ridge as the posterior barrier. Construction of a bidirectional block to conduction between these two barriers by means of lesions created with radiofrequency current have been shown to be effective in ablating the flutter. We now find that surgical creation of such a block to conduction between the barriers by a simple modification of the atrial incision line is equally effective. In a 6-year-old boy, who was admitted to our hospital for closure of an atrial septal defect and treatment of sustained atrial flutter, the atriotomy was performed perpendicular to the terminal groove and extended towards the tricuspid annulus, placing some cryothermal lesions between the end of the incision and the annulus. The septal defect was closed using a Dacron patch. The child was free of arrhythmia both during the postoperative stay and over the initial three months of follow-up. We conclude that this simple modification of the atrial incision line provides cure of atrial flutter in children who require atriotomy for repair of congenital cardiac anomalies. It may also be beneficial in preventing 'incisional' reentrant tachycardia.

Atrial Flutter↗

Conversion of atrial flutter in pediatric patients by transesophageal atrial pacing: a safe, effective, minimally invasive procedure.

Atrial reentry tachycardia, often termed atrial flutter, is an arrhythmia that is uncommon in the general pediatric population but is seen frequently in patients with congenital heart disease. One goal in treating the arrhythmia is to terminate it, returning the atrium to its underlying rhythm. This report describes the use of transesophageal atrial pacing to attempt termination of atrial reentry in 102 pediatric patients (158 episodes). The patients ranged in age from 1 hour to 41.5 years. Conversion was successful for 112 (71%) of 158 episodes. Six of the 112 episodes required an infusion of procainamide after initial attempts at pacing led to atrial fibrillation. There were no significant differences between the ages of patients or the duration of the tachycardia in comparing successful versus unsuccessful conversions. In contrast, the atrial cycle lengths for the successfully converted tachycardias were significantly greater than for unsuccessful attempts. Transesophageal atrial pacing is a safe and effective means of terminating atrial flutter in the pediatric population. It is minimally invasive, it can often be performed in an outpatient setting, and the technique may occasionally be facilitated by infusion of intravenous procainamide.

Adolescent↗

Pharmacologic versus direct-current electrical cardioversion of atrial flutter and fibrillation.

Conversion of atrial flutter and atrial fibrillation (AF) can be achieved by either pharmacologic or direct-current (DC) electrical cardioversion. DC electrical cardioversion is more effective and restores sinus rhythm instantaneously; however, general anesthesia is necessary, which can cause severe complications. On the other hand, pharmacologic cardioversion is less effective. First, time to conversion is unpredictable and may be relatively long, especially with oral drug therapy. Also, the rate of conversion is lower and depends on duration of AF. In addition, safety is an important issue. Adverse drug reactions include bradycardia, paradoxical tachycardia due to enhanced atrioventricular conduction, ventricular proarrhythmia, and acute heart failure. In paroxysmal AF, drug therapy is usually aimed at an acute conversion. Class IA and IC drugs are more efficacious than the class III drugs sotalol, amiodarone, and ibutilide. By contrast, class III drugs are more effective for the conversion of atrial flutter. Acute conversion out-of-hospital ("pill in the pocket approach") should be done only if the drug used appeared effective and safe after a few in-hospital trials. In persistent AF, DC conversion is preferred because drugs are particularly ineffective if the arrhythmia has lasted >24-48 hours. The latter probably relates to electrical and anatomical remodeling of the atria during ongoing atrial fibrillation and flutter. Nevertheless, a wait-and-see approach using, for example, oral amiodarone may be adopted with late DC conversion if the drug fails to convert persistent AF. However, the consequences of remodeling seem to dictate an early conversion. In this respect, echocardiography-guided DC cardioversion may become increasingly important in AF. It will prevent treatment resistance and potentially reduces embolic complications. In a hybrid approach, antiarrhythmic drugs may be used to enhance DC conversion and prevent (sub)acute recurrences of AF. However, it may increase the defibrillation threshold, especially if class IC drugs are used. New treatment options such as automatic defibrillation (implantable atrioverter) are still investigational.

Ambulatory Care↗

[1/1 nodo-ventricular conduction atrial flutter with amiodarone].

1/1 atrial flutter is a regularly described complication of class I anti-arrhythmics. It is, however, very rarely encountered with class III anti-arrhythmics because prolongation of the atrio-ventricular node refractory period prevents 1/1 nodo-ventricular conduction. There have only been seven cases of 1/1 atrial flutter with amiodarone reported in the literature. Here we describe a new case of 1/1 atrial flutter with amiodarone. Our case clearly illustrates not only the different pro-arrhythmic effects of amiodarone (prolongation of the flutter cycle, and infra-Hissian block) but also the pathophysiological mechanisms possible with 1/1 conduction (prolongation of the flutter cycle, considerable permeability of the AV node). It demonstrates the difficulties of diagnosing such a rhythm disturbance, and that it is sometimes poorly tolerated, as well as underlining the importance of early diagnosis (in this case by oesophageal recording). Preventive treatment of 1/1 flutter can include amiodarone, digitalis, a betablocker or a bradycardic calcium inhibitor.

Aged↗

The risk of atrial fibrillation following radiofrequency catheter ablation of atrial flutter.

BACKGROUND: Although radiofrequency catheter ablation of atrial flutter is associated with a high rate of initial success, several clinical issues regarding this therapy remain to be defined. For example, the risks of recurrent atrial flutter and of developing atrial fibrillation after flutter ablation are unknown. In addition, it is not known whether elimination of atrial flutter will modify the natural history of atrial fibrillation in patients who experience both of these arrhythmias. The purpose of the present study was to determine the actuarial freedom from recurrent or new atrial arrhythmias in patients with atrial flutter undergoing catheter ablation. METHODS AND RESULTS: The study population consisted of 59 consecutive patients (mean age, 61.9 +/- 12.6 years) with typical atrial flutter who underwent catheter ablation of the reentrant circuit. Catheter ablation was not advised for patients in whom paroxysmal atrial fibrillation had been a major clinical problem. The inducibility of atrial fibrillation and atrial flutter was assessed after successful atrial flutter ablation with programmed atrial stimulation and rapid atrial pacing to a cycle length of 180 ms or 2:1 atrial capture. Atrial flutter was successfully ablated and rendered noninducible in 53 of 59 patients (90%). Over a mean follow-up period of 13.2 +/- 6.6 months, atrial flutter recurred in 5 patients (9.4%). Atrial fibrillation occurred in 14 of 53 patients after successful ablation (26.4%). Four clinical variables were associated by univariate analysis with the late occurrence of atrial fibrillation: (1) the presence of structural heart disease, (2) a history of atrial fibrillation before ablation of atrial flutter, (3) inducible sustained atrial fibrillation after ablation, and (4) a greater number of failed antiarrhythmic drugs. By multivariate analysis, only the persistent inducibility of sustained atrial fibrillation predicted the later development of atrial fibrillation. CONCLUSIONS: Although atrial flutter ablation is highly effective and associated with a low risk of recurrent atrial flutter, atrial fibrillation continues to be a long-term risk for individuals undergoing this procedure. The risk of later atrial fibrillation is especially high for patients in whom sustained atrial fibrillation remains inducible after ablation of atrial flutter.

Aged↗

P loops during common and uncommon atrial flutter in man.

Atrial flutter has never been satisfactorily defined. The 'common' pattern of flutter was originally described by Lewis in 1913. Less frequently observed forms of flutter are termed 'uncommon'. Sixteen cases of the 'common' and 6 of the 'uncommon' type have been studied using isolated P loop vectorcardiography. All patients had some degree of atrioventricular block but none had evidence of digitalis excess. The atrial rates were regular and were in a range between 250 and 330/minute. Vagal manoeuvres increased AV block in each instance. All those with the 'common' type of flutter had P loops with a caudad-cephalad orientation and fifteen of the sixteen had forces which descended over the right atrium and ascended over the left atrium. The 6 cases of the uncommon type of flutter had rates which ranged between 250 and 300/minute and did not fulfil both of the criteria for 'common' flutter; namely continuous baselineu ndulation and prominent negative P deflections in the inferior leads. The cases with the 'uncommon' type of flutter had a variety of loop patterns. The most frequent type was oriented inferior slightly to the right and anterior. One patient satisfied criteria for left atrial flutter. In another the loop was oriented inferior leftward and anterior. The vectorcardiogram provides a rich source of descriptive data but does not identify the underlying mechanism(s) of flutter.

Aged↗

Left atrial appendage function in patients with atrial flutter.

OBJECTIVE: To determine whether echocardiographic markers thromboembolic risk differ between patients with pure atrial flutter and patients with atrial flutter and intermittent atrial fibrillation. DESIGN: Patients with atrial flutter were followed up prospectively for 12 months to identify intermittent atrial fibrillation. After the follow up period, transthoracic and multiplane transoesophageal echocardiography were performed to assess left atrial chamber and appendage size, peak emptying velocities, and emptying fraction of the left atrial appendage. The presence of spontaneous echo contrast was also determined. SETTING: Tertiary cardiac care centre. PATIENTS: 20 consecutive patients with atrial flutter; 11 healthy subjects in sinus rhythm served as controls. RESULTS: Intermittent atrial fibrillation was documented in 11 patients by Holter monitoring or surface ECG; atrial fibrillation was not found in the other nine patients. Compared with the patients with pure atrial flutter, patients with atrial flutter and intermittent atrial fibrillation had larger left atrial chamber (mean (SD) 4.5 (0.6) v 3.8 (0.5) cm; 95% confidence interval 0.2 to 1.2; P = 0.01) and appendage areas (6.7 (2.2) v 4.8 (4.9) cm; 95% CI 0.4 to 3.5; P = 0.02), lower left atrial appendage emptying fractions (33 (11)% v 52 (11)%; 95% CI 8 to 29; P = 0.008), and also lower left atrial appendage emptying velocities (0.44 (0.21) v 0.79 (0.27) m/s; 95% CI 0.13 to 0.56; P = 0.005). In addition, a higher incidence of spontaneous echo contrast (11% v 36%) was observed in patients with atrial flutter and intermittent atrial fibrillation. CONCLUSIONS: Left atrial appendage function is depressed and spontaneous echo contrast more frequent in patients with atrial flutter and intermittent atrial fibrillation, as opposed to patients with pure atrial flutter. These data support the concept that patients with atrial flutter and intermittent atrial fibrillation have an increased risk of thromboembolic events and should therefore receive adequate anticoagulant treatment.

Aged↗

Atrial flutter update.

Typical atrial flutter has long been considered a reentrant arrhythmia, but it is only recently that the full structure of the right atrial circuit was understood, leading to de devise of ablation techniques. Recognition of the role of functional block, based on anisotropic conduction was crucial to understanding of the flutter circuit. Anisotropy at the terminal crest creates a line of block that, with the orifices of superior and inferior vena cava, constitutes the posterior boundary of the flutter circuit. The anterior boundary is the tricuspid ring, and the circuit is a ring of myocardium made by the septal and anterior right atrial walls, linked on top by the right atrial roof and inferiorly by the inferior vena cava-tricuspid ring isthmus. This isthmus, a relatively narrow part of the circuit, has become the established target for typical flutter ablation. Complete, bidirectional isthmus block is the final goal of flutter ablation. This has to be assessed, after flutter interruption, by pacing both sides of the ablation line while recording electrogram sequences from the opposite right atrial wall and the isthmus itself. Success is great in terms of prevention of flutter recurrence, however a 30% incidence of atrial fibrillation during follow-up casts a large shadow on long-term prognosis. Understanding of the myocardial abnormalities underlying atrial flutter and fibrillation will be necessary to improve this long-term outlook.

Anticoagulants↗

Usefulness of the polarity in high-density wide range-filtered bipolar mapping to detect isthmus block during radiofrequency ablation of typical atrial flutter.

BACKGROUND: The atrial activation sequence around the tricuspid annulus (TA) cannot always be used to establish whether complete block has been achieved across the cavotricuspid isthmus (CTI) during radiofrequency ablation (RFCA) for typical counterclockwise atrial flutter (CCW-AFL). AIM: We examined whether a change in the polarity of the atrial high-density wide range-filtered bipolar electrograms recorded near the ablation line is an accurate indicator of complete CTI block. METHODS: Nineteen patients with CCW-AFL underwent RFCA. Electrograms were recorded around the TA with duodecapolar conventional (2mm x 8mm x 2mm spacing) and high-density (2-mm spacing) Halo catheters. The bipolar electrograms on the high-density Halo catheter recorded from a series of adjacent electrode pairs positioned just lateral to the ablation line were filtered at a bandpass setting of 0.05-500 Hz. The activation sequence on the conventional Halo catheter during coronary sinus pacing (CSp) and inferolateral TA pacing, and the bipolar electrograms on the high-density Halo catheter during CSp were determined before and after RFCA. The final complete CTI block was verified by the presence of widely split double electrograms > or =100 msec along the ablation line. RESULTS: The final complete CTI block was achieved in all the 19 patients. Before RFCA, the polarity of bipolar electrograms was predominantly negative during CCW-AFL and positive during CSp. In 18 of the 19 patients, the bipolar electrograms exhibited the CCW activation and a negative polarity during CSp only after complete CTI block. In one of those 18 patients, additional applications of RFCA changed the polarity of bipolar electrograms positive to negative although the conventional Halo electrogram activation sequence suggested complete CTI block during CSp. In seven patients, who had transverse conduction across the crista terminalis during CSp, the conventional Halo electrogram activation sequence suggested an incomplete CTI block. However, in six of those seven patients, the CCW activation had a predominantly negative polarity of the bipolar electrograms. In one of those seven patients, complete CTI block was unable to be detected even using the high-density Halo catheter. CONCLUSIONS: These data demonstrate that the high-density wide range-filtered mapping can identify the CTI block in undetectable cases of complete CTI block or incomplete CTI block by the conventional method. The polarity of the bipolar electrograms recorded just lateral to the ablation line during CSp after RFCA of AFL may be used as a simple and an accurate indicator of complete CTI block.

Adult↗