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Long-term efficacy of cryo catheter ablation for the treatment of atrial flutter: results from a repeat electrophysiologic study.

OBJECTIVES: We investigated the long-term efficacy of cryo ablation for treatment of atrial flutter. BACKGROUND: To our knowledge, no study has assessed the long-term efficacy of cryo ablation by assessing both symptom and conduction recurrence. METHODS: A total of 45 consecutive patients with symptomatic atrial flutter were ablated with a 7-F, 6-mm-tip, quadripolar cryo catheter (Freezor Xtra, CryoCath Technologies Inc., Kirkland, Canada). Electrophysiologic studies (EPS) were performed with diagnostic catheters. Cryo ablation was at -75 degrees C for 4 min, beginning at the inferior rim of the coronary sinus os and creating a posterior line to the Eustachian ridge. Safety, bi-directional isthmus block at intervention, and recurrence at three, six, and nine months post procedure were assessed. RESULTS: There were no adverse events reported. All patients were free of discomfort on cryo energy delivery. The acute success rate at intervention was 87%. Follow-up data from 39 acutely successful patients showed 27 (69%) without conduction recurrence on repeat EPS at three months, and none (0%) had symptom recurrence documented by Holter monitoring, electrocardiogram, and/or patient diary records at three, six, and nine months follow-up. CONCLUSIONS: Our experience with a new 7-F, 6-mm-tip, quadripolar cryo catheter yielded a fairly high success rate at intervention, an excellent safety profile, and a good chronic success rate in terms of symptom recurrence. However, further monitoring is necessary to determine whether all asymptomatic patients continue to remain free of symptoms, given the small pool of patients demonstrated to have conduction recurrence.

Aged↗

The role of catheter ablation techniques in the treatment of classic (type 1) atrial flutter.

Several attempts at circuit interruption of type 1 atrial flutter by means of surgical or catheter techniques have been published. We recently reported the results of a series of patients who underwent catheter fulguration of the low septal right atrium, with a mean follow-up of almost 3 years. True electrophysiological success was observed in 7/14 patients (50%). Clinical success, defined as absence of symptoms, was observed in 8 was observed in 8/14 (57%) in this patient population. No serious complications were encountered, but the potential risks of DC shock, and the experience that we gained in right atrial mapping using this approach, led us to reconsider the role of atrial DC ablation in these patients. Additional studies assessing the meaning of fragmented electrograms, and identification of one (or of several) slow conduction areas of the reentrant circuit are ongoing.

Atrial Flutter↗

Atrial flutter in the perinatal age group: diagnosis, management and outcome.

OBJECTIVES: The aim of this retrospective study was to evaluate perinatal atrial flutter (AF) and the efficacy of maternally administered antiarrhythmic agents, postpartum management and outcome. BACKGROUND: Perinatal AF is a potentially lethal arrhythmia, and management of this disorder is difficult and controversial. METHODS: Forty-five patients with documented AF were studied retrospectively. RESULTS: Atrial flutter was diagnosed prenatally in 44 fetuses and immediately postnatally in 1 neonate. Fetal hydrops was seen in 20 patients; 17 received maternal therapy, 2 were delivered and 1 was not treated because it had a severe nontreatable cardiac malformation. In the nonhydropic group of 24 patients, 18 were treated and the remaining 6 were delivered immediately. In the hydropic group, 10 received single-drug therapy (digoxin or sotalol) and 7 received multidrug therapy. In the nonhydropic group, 13 received a single drug (digoxin or sotalol) and 5 received multiple drugs. One patient with rapid 1:1 atrioventricular conduction (heart rate 480 beats/min) died in utero and another died due to a combination of severe hydrops because of the AF, sotalol medication, stenosis of the venous duct and hypoplastic placenta. Of the 43 live-born infants, 12 were in AF at birth. Electrical cardioversion was successful in eight of nine patients. No recurrences in AF have occurred beyond the neonatal period. Four patients with fetal flutter and hydrops showed significant neurological pathology immediately after birth. CONCLUSIONS: Fetal AF is a serious and threatening rhythm disorder, particularly when it causes hydrops, it may be associated with fetal death or neurological damage. Treatment is required and primarily aimed at reaching an adequate ventricular rate and preferably conversion to sinus rhythm. Digoxin failed in prevention of recurrence at time of delivery in a quarter of our patients, whereas with sotalol no recurrence of AF has been reported, suggesting that class III agents may be the future therapy. Once fetuses with AF survive without neurological pathology, their future is good and prophylaxis beyond the neonatal period is unnecessary.

Anti-Arrhythmia Agents↗

Atrial flutter with inapparent flutter waves on the surface electrocardiogram.

A case with inapparent flutter waves on surface electrocardiogram are described. Typical atrial flutter activity could be seen on right atrial monophasic action potential recordings, His bundle electrograms and echocardiograms. During long pauses induced by carotid sinus massage the atrial activity on endocavitary tracings and echocardiograms was unchanged while isoelectric lines were recorded on the twelve surface electrocardiographic leads.

Adolescent↗

Effects of class IA antiarrhythmic drugs on the reentrant circuit in common human atrial flutter.

In 9 patients with the common type of atrial flutter (AF), a zone of slow conduction was observed proximal to the coronary sinus orifice. Class IA antiarrhythmic drugs were administrated intravenously in all 9 patients. AF was converted to sinus rhythm in only 1 patient. In the remaining 8 patients, although IA drugs suppressed conduction velocity, this effect was not preferential with regard to the zone of slow conduction. Conversion of AF to sinus rhythm by rapid pacing was achieved in these 8 patients. At a critical pacing cycle length, AF was interrupted just after conduction block developed in the zone of slow conduction. A progressive decrease in conduction velocity was observed in the zone of slow conduction for several beats just before the onset of conduction block. In conclusion, class IA drugs facilitate the interruption of AF by rapid atrial pacing by inducing conduction block in the zone of slow conduction.

Adult↗

Anatomy of the tricuspid annulus. Circumferential myofibers as the structural basis for atrial flutter in a canine model.

BACKGROUND: Little anatomic information is available on the annular myocardium. This study was conducted to determine the anatomic substrate for atrial flutter due to circus movement around the tricuspid annulus in the Y-shaped incision canine model of atrial flutter. METHODS AND RESULTS: We studied photographs of the annular myocardium serial histological sections, made in either of three different planes, and compared these with photographs of the intact and blocked gross heart specimens. We found that the annulus is the most caudal region of the atrial wall. The epicardial aspect of the annulus abuts the ventricular septum or the aortic root in the medial region; in other regions, it is covered by the fat of the coronary sulcus. Its endocardial aspect is delimited by the tricuspid leaflets inferiorly and by the pectinate muscle bundles superiorly, except in the medial region where the pectinate muscle bundles are absent. The annular myocardium is bilaminated. A continuous subepicardial circumferential lamina is the most prominent and is robust in the anterior, lateral, and posterior regions, but it attenuates to a fine muscular connection in the medial region. Myofibers of its superior border merge with the pectinate muscle bundles or are admixed in the medial region with myocardium at the base of the medial atrial wall. Its inferior border makes little contact with the annulus fibrosus about the ring; however, in the medial region, these myofibers insert into fibrous tissue superior to the septal leaflet. A discontinuous, subendocardial perpendicular lamina contains myofibers that descend from the atrium; most of these myofibers insert into the annulus fibrosus about the ring, but the lamina is absent in the anteromedial region. CONCLUSIONS: We conclude that the continuous circumferential lamina provides the anatomic substrate for circus movement of excitation in this model.

Animals↗

[Atrial flutter: causes, electrophysiological characteristics, treatment with radiofrequency catheter ablation].

Atrial flutter (TP) is one of the most common supraventricular tachyarrhythmias. Because of its influence on hemodynamics of the circulation, prolonged episode of paroxysmal TP can lead in as many as 1/3-1/2 patients to clinical signs of coronary insufficiency, decompensation of the circulatory system, or even such life-threatening states, like cardiac arrest. Patients with preexcitation syndrome, hyperthyroidism, as well as children, whose atrio-ventricular (AV) node can conduct in a 1:1 fashion, are in the group of particularly high risk of complications. Recurrent episodes of TP are also associated with frequent occurrence of thromboembolic events. Based on the electrocardiographic (ECG) pattern TP is divided into common type, with negative "sawtooth" in leads II, III, aVF, and uncommon type, which is characterised by other ECG morphologies. Experimental and clinical data have revealed, that common and some part of uncommon type are due to clockwise or counterclockwise reentry in the right atrium. These forms of TP can be treated with high success-rate with radiofrequency (CR) ablation. Because of difficulties in pharmacological conversion of the arrhythmia to the sinus rhythm and high frequency of recurrences, CR ablation seems to be a high effective method of treatment in patients with common and some forms of uncommon TP.

Atrial Flutter↗

Atrial fibrillation and atrial flutter.

The epidemiology, pathophysiology, diagnosis, evaluation, and treatment of atrial fibrillation (AF) and atrial flutter (AFl) are reviewed, and recent developments and controversies in the approach to these arrhythmias are addressed. AF and AFl are the arrhythmias most frequently encountered in clinical practice. Although occasionally unaware of their arrhythmia, patients usually complain of palpitations, weakness, dyspnea, and decreased exercise tolerance. The initial goal of therapy is control of the ventricular rate. Rate control is accomplished with atrioventricular node-blocking agents such as digoxin, calcium-channel blockers, or beta-adrenergic blockers. Along with a rapid, irregular ventricular response, other detrimental outcomes of AF and AFl include compromised hemodynamics and increased vulnerability to thromboembolism. After the cause of the patient's arrhythmia has been evaluated, pharmacologic treatment is directed at converting the rhythm to normal sinus rhythm and maintaining it. Antiarrhythmic drugs have proved effective in about 50% of cases but may be associated with increased mortality. More effective and safer forms of drug therapy for AF and AFl are needed. Nonpharmacologic alternatives to antiarrhythmic medications for refractory AF and AFl include radio-frequency catheter ablation of the bundle of His with pacemaker placement and surgery. Patients who remain in AF despite therapy should receive long-term warfarin treatment. Drugs may be used to control the ventricular response in patients with AF and AFl, terminate and prevent the arrhythmias, and prevent thromboembolism. Nonpharmacologic treatments are reserved for patients whose arrhythmias are poorly controlled by drugs.

Adrenergic beta-Antagonists↗

Using intracardiac catheter recordings from the His and proximal coronary sinus to distinguish isthmus conduction block during catheter ablation of type I atrial flutter.

Isthmus conduction block, demonstrated with the use of multipolar catheter recordings, is considered the preferred endpoint for ablation of type I atrial flutter. This study investigated the feasibility of using recordings from the His and coronary sinus (CS) to document isthmus conduction block. Isthmus conduction block was produced with linear radiofrequency (RF) ablation in 27 patients with type I atrial flutter. In 13 patients (group I), RF was delivered until bidirectional isthmus conduction block was demonstrated with multipolar Halo catheter recordings. In 14 patients (group II), RF was delivered during pacing from the lateral isthmus at 600 ms until a reversal in activation of the proximal CS and His occurred. At this point, data from the Halo recordings were reviewed to see if reversal correlated with conduction block; if not, further ablation was performed until block was demonstrated. The initial reversal in His and CS activation during RF energy delivery correlated with isthmus block in only 4 (28.6%) of 14 patients in group II. Additional RF delivery produced isthmus block in the other ten patients resulting in a further increase in the St-CS interval of 35 +/- 20 ms. A His-CS interval of at least -40 ms signified isthmus block with a sensitivity and specificity of 48% and 100%, respectively. Reversal in His-CS activation during pacing from the lateral margin of the isthmus is not specific for the creation of isthmus block. While activation of the proximal CS bipole > 40 ms after activation of the His appears specific for isthmus block, the low sensitivity of this finding limits its clinical use.

Atrial Flutter↗

Acute coronary occlusion during radiofrequency catheter ablation of typical atrial flutter.

We report the first case of acute right coronary artery occlusion in an adult patient during radiofrequency catheter ablation of typical atrial flutter. ST segment elevation rapidly resolved with antithrombotic therapy. This complication was thought to be due to the short distance between the endocardium and the right coronary artery at the ablation site, the high-wattage output from the radiofrequency generator, and the lack of sufficient cooling effect related to a severe upstream coronary stenosis. In patients with known right coronary artery stenosis who are suffering from typical atrial flutter, evaluation of the significance of the stenosis would be reasonable.

Acute Disease↗

Progressive isthmus delay during atrial flutter ablation: the critical importance of isthmus spanning electrodes for distinguishing pseudoblock from block.

Bidirectional isthmus block is associated with successful atrial flutter ablation, whereas creation of increased isthmus conduction delay without block can be proarrhythmic. Often, halo catheter electrodes fail to provide adequate sub-Eustachian isthmus recordings. The aim of this study was to determine if progressive isthmus conduction delay results in the false appearance of block during atrialflutter ablation. A 20-pole deflectable catheter was prospectively positioned across the sub-Eustachian isthmus (from the coronary sinus os [CSO] to 7:00 on the tricuspid valve annulus [TVA] clock face in the left anterior oblique [LAO] projection) in nine patients undergoing atrial flutter ablation. During sinus rhythm, conduction time was measured from the CSO to the 7:00 position while pacing the CSO. Measurements were repeated after each linear lesion and after conduction block was achieved. Transisthmus conduction time at baseline, just prior to success, and after the presence of complete block was 54 +/- 9, 123 +/- 39, and 155 +/- 30 ms, respectively (P < or = 0.01). The marked delay prior to complete block resulted in reversal of the activation sequence in electrodes at TVA 7:00, creating the false appearance of isthmus block; the isthmus electrodes clearly distinguished delay from block. Catheter ablation results in progressive isthmus conduction delay prior to the creation of complete block. Electrodes spanning the isthmus and line of block are critical for distinguishing conduction delay (and pseudoisthmus block) from block.

Adult↗

Effects of procainamide on the excitable gap composition in a canine model of atrial flutter.

The effects of increasing concentrations of procainamide on the composition of the excitable gap were determined in a canine model of atrial flutter. Using the model of a Y-shaped lesion in the right atrium, reentry around the tricuspid valve was induced by burst pacing in 10 open-chest chloralose-anesthetized dogs. Diastole was scanned with a single premature stimulus and the relationship between the coupling interval of the premature beat and the return cycle length (CL) determined a reset-response curve that described the excitable gap. This was repeated up to the maximum flutter CL while infusing procainamide (30 mg/kg) over 1 h. Procainamide progressively prolonged the flutter CL from 131 +/- 21 (+/-SD) to 188 +/- 46 ms (p < 0.01) and the effective refractory period from 96 +/- 19 to 149 +/- 47 ms (p < 0.01). At peak plasma levels of 77 +/- 33 mumol/L the drug terminated flutter only in two dogs. Neither the duration (35 +/- 10 to 39 +/- 13 ms) nor the composition of the excitable gap changed on drug. A fully excitable portion (7 +/- 3 ms or 20 +/- 11% of the excitable gap) persisted on procainamide (7 +/- 3 ms or 19 +/- 9% of the excitable gap). It was concluded that procainamide prolongs the atrial flutter CL and the effective refractory period but does not change either the duration or composition of the excitable gap even at plasma concentrations that significantly exceed those recommended in man.

Action Potentials↗

[Fetal atrial flutter in complete atrioventricular canal and trisomy 18].

Fetal supraventricular tachyarrhythmias are very rarely associated with congenital heart diseases. Usually a circus movement (= reentry), often associated with a preexcitation, and occasionally an atrial ectopic focus are suggested as the pathophysiologic mechanisms of supraventricular tachyarrhythmias. In the reported case - atrial flutter, complete common atrioventricular canal with fetal trisomy 18 - the atrial flutter was probably provoked by the dilatation of the atria due to the regurgitation of both atrioventricular valves. This case indicates the need for a detailed echocardiographic examination (using two-dimensional, M-mode, and Doppler-echocardiography) in each case of fetal tachyarrhythmias in order to exclude associated cardiac defects, possibly in association with a chromosomal anomaly.

Adult↗

Reentry circuit location and left atrial three-dimensional activation patterns in left atrial flutter.

We report the case of a patient with left atrial flutter (LAF) in whom the reentry circuit location was mapped with a 64-electrode basket catheter deployed in the left atrium. Left atrial three-dimensional activation patterns were constructed with a software program and presented as color-coded isochrones. The reentrant activation traveled preferentially around the mitral annulus in a clockwise direction. It consisted of a single reentry confined anteriorly by the mitral annulus and posteriorly by an anatomic-functional barrier composed of a functional conduction block extending between pulmonary veins and surrounding a part of the posterior wall of the left atrium. The lower portion of the posterior wall and the anterior wall in close proximity to mitral annulus were preferentially used by the reentrant impulse.

Atrial Flutter↗

Ablation of typical atrial flutter using a three-dimensional ultrasound mapping system.

AIMS: The aim of the study was to test the feasibility of the new Realtime Position Management mapping system for ablation of typical atrial flutter. METHODS AND RESULTS: The ultrasound multi-transducer catheters of the RPM Mapping System are placed in the coronary sinus and at the right ventricular apex. Position and movement of the ablation catheter can be depicted on the monitor at any time. Several guiding marks are set in the right atria and thus, define the subsequent lesion lines. A total of 15 patients were treated. In 13 patients complete bi-directional block was established after the ablation. In two patients only significant conduction delay was measured after the end of the procedure. A total of 10.2 +/- 6.3 cooled RF-applications were needed to reach the end-point of the procedure. The total energy was 18.76 +/- 13.23 J. The fluoroscopy time for ablation was 22.2 +/- 8.34 min. During a mean follow-up of 8.4 +/- 3.2 months no recurrence of atrial flutter occurred. One patient developed atypical flutter and another patient had atrial fibrillation. Both patients were treated with antiarrhythmic drugs. There was one ablation related complication, a pericardial effusion. CONCLUSION: The Realtime Position Management system is easy to manage and control. The precision of anatomical linear lesions is improved and fluoroscopic exposure time considerably reduced after learning curve.

Adult↗

Mixed fluoxetine/loxapine overdose and atrial flutter.

A 19-year-old man who attempted suicide by ingesting approximately 600 mg fluoxetine (Prozac) and 140 mg loxapine (Loxitane) had two episodes of atrial flutter shortly thereafter. Admission serum fluoxetine, norfluoxetine, and loxapine levels were 1,053 ng/mL, 702 ng/mL, and 40 ng/mL, respectively. This case of atrial flutter in association with an overdose of either of these drugs demonstrates the potential for cardiotoxicity with these agents in the overdose setting. Theoretical mechanisms of cardiotoxicity are presented.

Adult↗