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Role of pectinate muscle bundles in the generation and maintenance of intra-atrial reentry: potential implications for the mechanism of conversion between atrial fibrillation and atrial flutter.

To determine the role of pectinate muscle (PM) bundles in the formation of intra-atrial reentry, 10 isolated canine right atrial tissues were perfused with Tyrode's solution containing 1 to 2.5 micromol/L acetylcholine (ACh). The endocardium was mapped using 477 bipolar electrodes with 1.6-mm resolution. Reentry was induced by a premature stimulus (S2). Computer simulation studies were used to investigate the importance of regional myocardial thickness in reentry formation. A total of 40 episodes of reentry were induced; 28 episodes were stationary, and the remaining 12 were nonstationary. The stationary reentry was induced either immediately after the S2 stimuli (n=9) or after an initial period of irregular activations that lasted 1460+/-1077 ms (n= 19). Of 28 episodes, 20 were initiated by conduction block along large PM ridges, leading to wave break and the initiation of reentry. The reentrant wave fronts remained stationary and rotated around these ridges as anchoring sites. During the transition from the initial irregular activations to stationary reentry, the electrogram morphology converted from "fibrillation-like" to "flutter-like" activity. In 8 episodes, initially stationary reentry converted to irregular activations because of interference with outside wave fronts (n=5) or spontaneous separation of waves from the ridges (n=3). Compared with stationary reentry, nonstationary reentry always occurred over an area without large PMs, and the mean life span was much shorter (102+/-151 versus 3.8+/-1.1 rotations, P<0.001). Computer simulation studies showed that a critical ridge thickness is needed for reentry to anchor, thereby converting fibrillation to flutter. We conclude that PM ridge forms an area where wave break occurs, allowing the initiation of reentry. It also provides a natural anchor to the reentrant wave front, lengthening the life span of reentry. The attachment and detachment of the reentrant wave front to and from the ridge determine "flutter-like" or "fibrillation-like" activity.

Animals↗

Mechanisms of induction of typical and reversed atrial flutter.

INTRODUCTION: Typical flutter is due to reentry around caval veins and terminal crest. In patients with typical flutter, reversed (clockwise) reentry can be induced. We studied mechanisms of typical and reversed flutter induction. METHODS AND RESULTS: Thirteen patients (11 men) underwent 16 radiofrequency (RF) ablation procedures for typical (12) or reversed flutter (1). High right atrium (RA) stimulation included 1 to 3 extrastimuli over cycle lengths 600 to 250 msec, and burst. We recorded simultaneously from three levels of septal and anterior RA. RF was delivered to the inferior vena cava-tricuspid isthmus (CTI). Of 25 inductions, 4 were a result of single, 9 double, and 11 triple extrastimuli, and 1 burst. Clinical basal flutter was induced (7 typical, 1 reversed). After RF, typical flutter was reinduced in 9 cases and reversed flutter in 7, with only typical flutter seen clinically. All flutters were interrupted by ablation or catheter pressure on the CTI. Typical flutter began by low RA septal activation block, preceded by repetitive responses in 12 instances, atypical flutter in 1, and directly from stimuli in 4. Reversed flutter started in 8 instances by low RA block of a stimulated front descending the anterior wall and in 1 by repetitive responses. CONCLUSION: Septal activation block was the usual mechanism of typical flutter induction by RA extrastimuli. Facilitation of reversed flutter after RF application is probably due to a new area of block in the CTI. Flutter induction without intermediate rhythms confirms the presence of block at the terminal crest at baseline.

Atrial Flutter↗

Case report: Radiofrequency catheter ablation of typical atrial flutter and the atrioventricular junction via the superior vena caval approach in a patient with a congenital absence of an inferior vena cava.

The absence of an inferior vena cava is a rare congenital condition often without clinical significance. Alternative venous approaches are often needed to treat these patients. We report a case of successful ablation of both isthmus dependent flutter and the AV junction using the superior vena cava in a patient with an inferior vena cava anomaly.

Atrial Flutter↗

Histopathologic background for resistance to conventional catheter ablation of common atrial flutter.

Histopathologic examination of the cavotricuspid isthmus in which a large-tip catheter was necessary to achieve conduction block is presented. No thickened myocardium or prominent trabeculation was observed on the ablation line. A small cardiac vein extending through the isthmus across the ablation scar was detected. The remaining myocardial cells were distributed along the small cardiac vein. It is possible that the luminal blood flow of the small cardiac vein protects the surrounding atrial muscle from effective delivery of radiofrequency energy.

Aged↗

Atrial flutter with amoxapine: a case report.

The author describes a patient with preexisting heart disease who rapidly developed cardiac arrhythmia in association with the use of amoxapine. He calls attention to the potential for serious cardiac toxicity with this new drug.

Aged↗

Atrial flutter ablation: electrophysiological landmarks.

Understanding the configuration of the whole flutter circuit is for us the only valid parameter allowing the design of an ablation strategy. Fragmented or double electrograms may have different meanings in different parts of the circuit, and full activation mapping is the best clue to their interpretation. Correlation of anatomy with activation sequence will mark the best ablation target (isthmus) in each case. Multiple simultaneous recordings from the septum and right atrial anterior wall are very helpful to rapidly diagnose circular activation of the right atrium. In cases without this type of activation, coronary sinus recordings and the study of postentrainment cycles are helpful to localize the reentry circuit.

Atrial Flutter↗

An unusual cause of new-onset atrial flutter: primary cardiac lymphoma.

Primary cardiac lymphoma is a rare disease with a high mortality rate due to the advanced stage of myocardial involvement at presentation. The diagnosis is extremely difficult to make because of the rarity of the disease, variability of clinical manifestations, limited noninvasive diagnostic techniques available, and difficulties and/or delays in the use of invasive measures. The incidence of the disease is increasing, especially among immunocompromised patients, with those suffering from acquired immunodeficiency syndrome accounting for the greatest increase. We report the case of an immunocompetent 76-year-old black woman who presented with near-syncopal episodes. Transthoracic echocardiogram revealed a right atrial mass. Surgical resection was performed, and a diagnosis of large B-cell non-Hodgkin's lymphoma was made. Primary cardiac lymphoma should be considered in any patient with a cardiac mass. Prompt diagnosis and treatment of primary cardiac lymphoma is imperative for survival.

Aged↗

Could it be myotonic dystrophy? Myotonic dystrophy presenting with atrial flutter.

Myotonic dystrophy is a well recognised and well defined multisystem disorder which is inherited in an autosomal dominant fashion through a locus on chromosome 19. The disease itself is characterised by rigidity and degeneration of skeletal muscle, cataract formation, gonadal atrophy, frontal baldness and mental retardation. Like many inherited disorders there is a variable expression and so diverse clinical presentations can occur.

Adult↗

[Radiofrequency ablation of type I atrial flutter. Personal experience].

The cause of Afl-I is macroentry in the right atrium. The critical site of reentry is the narrow anatomical space in the isthmic region between the posterior part of the annulus of the tricuspid valve and the vena cava inferior (isthmus TA-IVC). Radiofrequency ablation (RF) of the isthmus TA-IVC is successful on average in 90% of patients. The best criterium for evaluation of short-term and long-term effect of RF ablation is a two-way block of conduction in the TA-IVC insthmus, created by RF ablation. In case of a relapse it is possible to repeat ablation. Although a proarrhythmic effect of ablation is not assumed, the cause of the higher frequency of atrial fibrillation is not known. The authors present their own experience with the treatment of Afl-I by RF ablation of the TA-IVC isthmus in a group of 18 patients. RF ablation was successful in 83.3% patients of the group, no complications were recorded. Late relapses of Afl-1 in three patients were resolved by repeated RF ablation which was successful. The results are comparable with results in other departments. Based on their own experience the authors consider ablation treatment of Afl-1 a safe and effective therapeutic method in a selected group of patients.

Atrial Flutter↗

Polyuria in paroxysmal tachycardia and paroxysmal atrial flutter and fibrillation.

When Paul Wood spoke about this to the British Cardiac Society in 1961, we were impressed by the originality of his work on a subject that so many had noticed but failed to investigate. A few months before his death in July 1962, when I asked him if his paper was ready for the journal, he said that he had not yet been able to get all the evidence he hoped for to establish the full explanation. Unfortunately, he had not the time to complete this. I have, therefore, tried to set out as clearly as possible the stage that he had reached. Maurice Campbell

Arrhythmias, Cardiac↗