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PubMed1996

Comparison of bipolar atrial electrogram amplitude in sinus rhythm, atrial fibrillation, and atrial flutter.

Automatic mode switching pacemakers revert to non-atrial tracking modes in response to sensed atrial tachyarrhythmias. It is unclear how atrial electrogram amplitudes in sinus rhythm compare to those during atrial tachyarrhythmias. In this study, peak-to-peak bipolar atrial electrogram amplitudes were measured during sinus rhythm and either atrial fibrillation or atrial flutter in 69 patients. The mean atrial electrogram amplitudes were 1.59 +/- 1.36 mV during sinus rhythm and 0.77 +/- 0.58 mV during atrial fibrillation (P < 0.0001) for 25 patients with atrial fibrillation and 1.81 +/- 2.07 mV during sinus and 1.5 +/- 1.81 mV (P < 0.0001) for 44 patients with atrial flutter. The mean electrogram amplitudes during both atrial fibrillation and flutter correlated significantly with amplitudes during sinus rhythm (R = 0.79, R = 0.94, respectively, both P < 0.0001). The coefficient of variance of individual electrogram amplitudes was greater in atrial fibrillation than sinus (P < 0.0001). By comparing 20th percentile electrogram amplitudes in atrial fibrillation and flutter to mean sinus amplitudes, intermittent very low electrogram amplitudes (< 0.3 mV) were more likely during atrial fibrillation and flutter if the mean sinus electrogram amplitudes were < 1.5 mV and < 0.5 mV, respectively (P < 0.01). Eightieth percentile electrogram amplitude values in atrial fibrillation and flutter were equally likely to exceed mean sinus amplitude values in respective patients. In conclusion, mean atrial electrogram amplitudes during atrial fibrillation and flutter are less than but correlated to sinus rhythm electrogram amplitudes. Very low amplitude individual electrograms during these atrial arrhythmias are associated with low mean sinus rhythm electrogram amplitudes. These findings may have implications for the programming of permanent dual chamber pacemakers in patients with paroxysmal atrial fibrillation and flutter.

Adolescent↗
PubMed1996

Dofetilide versus quinidine for atrial flutter: viva la difference!?

Dofetilide is more effective than quinidine to terminate atrial flutter in this animal model. It is also more capable of lengthening refractoriness more uniformly than quinidine. While the investigators describe local changes in refractoriness and dispersion of refractoriness and wavelength meticulously, it is not clear which, if any, of these properties cause flutter termination or influence reinduction. This report provides new insight into the electrophysiologic mechanisms of antiarrhythmic drugs used to treat atrial arrhythmias. Related investigations are needed to expand our knowledge of the actions of antiarrhythmic drugs, how these drugs affect critical portions of the reentrant circuit, and how to identify potential adverse effects of these agents. Application of these data may help guide the use of antiarrhythmic drugs and allow development of safer, and yet more potent, compounds. At least, it will give us pause about using more toxic and less effective drugs. While Class III drugs, specifically dofetilide, may be more potent and beneficial than quinidine in this model, it is uncertain that these results pertain to human reentrant atrial arrhythmias, particularly, atrial flutter. Perhaps dofetilide will be effective for certain types of atrial flutter requiring an anatomical center defined by an area of injury or surgical scar in the right atrium. The fact that these, and previous, data indicate a specific beneficial effect of dofetilide, particularly on atrial flutter, is interesting. Even if dofetilide proves highly effective for human atrial flutter, its safety will need to be proven in large clinical trials. The most obvious concern about dofetilide is development of serious side effects such as torsades de pointes. Clinical trials of this drug for atrial arrhythmias are presently ongoing. Ultimately, the long-term use of such a drug is dependent on the emergence of other highly effective therapies such as radiofrequency ablation.

Animals↗
PubMed2003

Thromboembolic risk of patients referred for radiofrequency catheter ablation of typical atrial flutter without prior appropriate anticoagulation therapy.

BACKGROUND: Radiofrequency catheter ablation of isthmus dependent atrial flutter is considered the therapy of choice. There is, however, controversy with regard to the thrombogenicity of atrial flutter in comparison with atrial fibrillation. METHODS: Consecutive patients scheduled for catheter ablation of documented typical atrial flutter receiving insufficient (INR < 2.0) or no anticoagulation during the three weeks preceding the procedure underwent multiplane transesophageal echocardiography (TEE). Patients with exclusive documentation of atrial flutter were classified as group I, whereas patients with additional documentation of atrial fibrillation were classified as group II. RESULTS: The study included 201 patients, 62 of whom were not on therapeutic anticoagulation (mean age 64 +/- 9 years, 87% men). In 10 of these 62 patients (16%), TEE detected a left atrial (LA) appendage thrombus in 4, or dense spontaneous echo contrast (SEC) in 6 patients. Comparison of patients with versus without SEC or thrombus, revealed a higher incidence of valvular heart disease (60% vs 26%, P = 0.05), but no differences with respect to age, gender, LA diameter, left ventricular end-diastolic diameter, or left ventricular ejection fraction. The incidence of positive TEE findings in group I was 1 in of 36 versus 9 of 26 in group II (3% vs 35%, P < 0.001), and the relative risk for thromboembolism in group II versus group I was 12.5 (95% CI: 3-55, P < 0.001). CONCLUSION: There is a significant risk for thromboembolism in patients referred for ablation of typical atrial flutter who have not been appropriately anticoagulated.

Anticoagulants↗
PubMed1997

Characterization of low right atrial isthmus as the slow conduction zone and pharmacological target in typical atrial flutter.

BACKGROUND: Previous electrophysiological studies in patients with typical atrial flutter suggested that the slow conduction zone might be located in the low right atrial isthmus, which is a path formed by orifice of inferior vena cava, eustachian valve/ridge, coronary sinus ostium, and tricuspid annulus. The conduction characteristics during atrial pacing and responses to antiarrhythmic drugs of this anatomic isthmus were unknown. METHODS AND RESULTS: Forty-four patients, 20 patients with paroxysmal supraventricular tachycardia (group 1) and 24 patients with clinically documented paroxysmal typical atrial flutter (group 2), were studied. A 20-pole halo catheter was situated around the tricuspid annulus. Incremental pacing from the low right atrium and coronary sinus ostium was performed to measure the conduction time and velocity along the isthmus and lateral wall in the baseline state and after intravenous infusion of procainamide or sotalol. In both groups, conduction velocity in the isthmus during incremental pacing was significantly lower than that in the lateral wall before and after infusion of antiarrhythmic drugs. Furthermore, gradual conduction delay with unidirectional block in the isthmus was relevant to initiation of typical atrial flutter. Compared with group 1, group 2 had a lower conduction velocity in the isthmus and shorter right atrial refractory period. Procainamide significantly decreased the conduction velocity, but sotalol did not change it. In contrast, sotalol significantly prolonged the atrial refractory period with a higher extent than procainamide. After infusion of procainamide, the increase of conduction time in the isthmus accounted for 52+/-19% of the increase in flutter cycle length, and 5 of 12 patients (42%) had spontaneous termination of typical flutter. After infusion of sotalol, typical flutter was induced in only 6 of 12 patients (50%) without significant prolongation of flutter cycle length. CONCLUSIONS: The low right atrial isthmus with rate-dependent slow conduction properties is critical to initiation of typical human atrial flutter. It may be the potentially pharmacological target of antiarrhythmic drugs in the future.

Adolescent↗
PubMed1994

Characterization of the excitable gap in a functionally determined reentrant circuit. Studies in the sterile pericarditis model of atrial flutter.

BACKGROUND: Single premature beats were introduced in the reentrant circuit during stable atrial flutter in the canine sterile pericarditis model to test the hypotheses that (1) despite the fact that the reentrant circuit is functionally determined, there is a fully excitable gap; (2) the excitable gap in the reentrant circuit is not uniform; and (3) inhomogeneities of conduction in the reentrant circuit explain the effects of premature beats. METHODS AND RESULTS: A multiplexing system was used to record 190 unipolar electrograms from the right atrial free wall during 18 atrial flutter episodes in 9 dogs. In all 18 episodes, premature stimuli captured the atrial flutter reentrant circuit. At the longest coupling intervals, the return cycle at the site closest to the pacing site did not prolong. As the coupling interval of the premature stimulus decreased, the return cycle then progressively increased, associated with changes in conduction in the reentrant circuit that were not uniform. The result was that coupling intervals associated with introduction of the premature beat also were not constant. The mean duration of the total (ie, fully plus partially) excitable gap was 12 +/- 4 ms in areas of slow conduction, and it was always shorter than the total excitable gap in other areas (22 +/- 6 ms, P < .001). The mean duration of the fully excitable gap based on analysis of the return cycle was 4 +/- 1 ms in the reentrant circuit. In 13 of 18 atrial flutter episodes, a premature stimulus terminated atrial flutter by causing block of the orthodromic wave front of the premature beat in an area of slow conduction. The mean coupling interval that caused orthodromic block was 113 +/- 5 ms (recorded at the site just proximal to the area of block), and it was always longer than the delivered stimulus coupling interval at the pacing site (96 +/- 8 ms, P < .001). CONCLUSIONS: We conclude that in this functionally determined atrial flutter reentrant circuit in the canine sterile pericarditis model, (1) a fully excitable gap is present in at least part of the reentrant circuit; (2) the duration of the excitable gap in the reentrant circuit is shortest in areas of slow conduction; and (3) when a premature beat encounters the partially excitable gap of the reentrant circuit, it results in changes in conduction such that the coupling intervals are not uniform throughout in the reentrant circuit.

Animals↗
PubMed1998

Atrial electrograms and activation sequences in the transition between atrial fibrillation and atrial flutter.

INTRODUCTION: The electrophysiologic mechanism of atrial fibrillation (AF) has a wide spectrum, and it seems that some atrial regions are essential for the occurrence of a particular type of AF. We focused on one type of AF: AF associated with typical atrial flutter (AFL), which was right atrial (RA) arrhythmia, and sought to investigate intra-atrial electrograms and activation sequences in the transition between AF and AFL. METHODS AND RESULTS: Intra-atrial electrograms and activation sequences in the RA free wall and the septum were evaluated in the transition between AF and AFL in seven patients without organic heart disease (all men; mean age 57+/-11 years). In five episodes of the conversion of AFL into AF, the AFL cycle length was shortened (from 211+/-6 msec in stable AFL to 190+/-15 msec before the conversion, P, 0.001). Interruption of the AFL wavefront and an abrupt activation sequential change induced by a premature atrial impulse resulted in fractionation and disorganization of the septal electrograms. During sustained AF, septal electrograms were persistently fractionated with disorganized activation sequences. However, the RA free-wall electrograms were organized, and the activation sequence was predominantly craniocaudal rather than caudocranial throughout AF. In 12 episodes of the conversion of AF into AFL, the AF cycle length measured in the RA free wall increased (from 165+/-26 msec at the onset of AF to 180+/-24 msec before the conversion, P, 0.001). AFL resumed when fractionated septal electrograms were separated and organized to the caudocranial direction, despite the RA free-wall electrograms remaining discrete and sharp with an isoelectric line. CONCLUSION: Changes of the electrogram and activation sequence in the atrial septum played an important role in the transition between AF and AFL.

Adult↗
PubMed1986

Atrial pacing for conversion of atrial flutter.

Fifty-seven episodes of atrial flutter in 46 consecutive medically treated patients (aged 60 +/- 17 years) were treated by rapid atrial pacing. Thirty-three patients (72%) had structural heart disease. Most pacing trials were conducted in patients receiving digoxin (88%) and antiarrhythmic drugs (77%). In 51 of 57 trials (89%), patients were successfully converted to normal sinus rhythm. Multivariate analysis revealed that patients who had congestive heart failure and who were older were more likely to be refractory to pacing. Left atrial size did not influence outcome. Confirmation of local atrial capture with a bipolar atrial electrogram and use of multiple atrial pacing sites enhanced the success rate. Eight patients (17%) demonstrated sinus node suppression after atrial pacing; sinus node disease was previously unsuspected in 4 of these patients. These bradyarrhythmias were easily managed because a pacing catheter was already in place. The only significant complication was femoral vein thrombosis in 1 patient. It is concluded that atrial pacing is an effective, safe and convenient method for the elective conversion of atrial flutter in the general population of medically treated patients. This technique is an attractive alternative to transthoracic cardioversion, and may be preferable in many patients.

Adult↗
PubMed2004

Electrophysiology of inducible atrial flutter in patients with atrioventricular nodal reentrant tachycardia.

An association between atrial flutter and atrioventricular nodal reentrant tachycardia (AVNRT) has been observed, but the underlying mechanisms are poorly defined. This issue was therefore investigated by comparing the electrophysiological properties of AVNRT patients with and without inducible atrial flutter and those of patients with a history of flutter. Twenty-nine patients with clinically documented atrial flutter and 104 with AVNRT were studied. Atrial flutter was induced in 38 (37%) AVNRT patients during standardized electrophysiological testing before radiofrequency ablation. The atrial relative refractory periods in AVNRT patients with inducible flutter (260 +/- 30 ms) were significantly shorter than those of either patients with a history of flutter (282 +/- 30 ms; P = 0.02) or AVNRT patients without inducible flutter (284 +/- 38 ms; P = 0.006). The atrial effective refractory periods in AVNRT patients with inducible flutter (205 +/- 31 ms) were shorter than in AVNRT patients without inducible flutter (227 +/- 40 ms; P = 0.01). The maximum AH interval during premature atrial stimulation in patients with clinical flutter (239 +/- 94 ms) was shorter than in AVNRT patients either with (290 +/- 91 ms; P = 0.04) or without inducible flutter (313 +/- 101 ms; P = 0.002). However, no significant differences were found in the maximum AH interval achieved during incremental atrial pacing among different groups. Our data show that a non-clinical flutter could more often be induced in those who had short atrial refractoriness. Despite their anatomical proximity, the slow pathway conduction of AVNRT and the isthmus slow conduction of flutter may be related to different mechanisms.

Atrial Flutter↗
PubMed1991

Usefulness of excitable gap and pattern of resetting in atrial flutter for determining reentry circuit location.

Clinical and experimental data show that type I atrial flutter is due to a reentry mechanism with an excitable gap. To define the location of the reentry circuit of atrial flutter, width of excitable gap, poststimulation cycle and pattern of reset after premature stimulus were analyzed in 18 patients during atrial flutter at multiple atrial sites (high, lateral, posterior and septal right atrium, and coronary sinus). The pattern of reset was defined as flat or increasing whether the return cycle remained unchanged or prolonged with increasing prematurity. Shorter values of the excitable gap were found at the coronary sinus (33 +/- 8 ms) and high right atrium (30 +/- 10 ms) than at the posterior (43 +/- 9 ms) or septal right atrium (45 +/- 11 ms). Intermediate values (36 +/- 8 ms) were measured at the lateral right atrium. Poststimulation cycle, corrected for atrial flutter cycle length, was shorter in the posterior (6 +/- 7 ms) and septal right atrium (5 +/- 7 ms) than in the coronary sinus (35 +/- 9 ms), and the high (23 +/- 10 ms) and lateral right atrium (15 +/- 9 ms). A flat pattern of resetting occurred more frequently at the septal (18 of 18 patients) and posterior right atrium (15 of 18) than at the lateral (8 of 18) and high right atrium (2 of 17), and was never observed at the coronary sinus. Atrial flutter was successfully terminated by overdrive atrial pacing in 15 of 18 patients, and termination was more easily obtained from the septal and posterior right atrium.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Flutter↗
PubMed2002

[Atrial flutter with 1/1 nodo-ventricular conduction with amiodarone. From physiopathology to diagnosis].

Atrial flutter with 1/1 nodo-ventricular conduction is a classical complication of Vaughan-Williams's Class I antiarrhythmic drugs. The increase of the flutter cycle and weak action of the antiarrhythmic on the atrioventricular node leads to 1/1 conduction of atrial depolarisation to the ventricles. In view of their marked action on the atrioventricular node, this type of pro-arrhythmic effect is very unexpected with Class III antiarrhythmics. The authors report 7 cases of 1/1 atrial flutter with oral amiodarone observed between 1994 and 2001. The patients were 6 men and 1 woman with an average age of 58 +/- 14 years. Four of them had underlying cardiac disease; none were hyperthyroid. The initial arrhythmia was 2/1 atrial flutter (n = 4), 1/1 atrial flutter (n = 2) and atrial fibrillation (n = 1). Treatment was preventive with doses of 400 mg/day associated with carvedilol in one patient and 200 mg/day in another. The other five patients all received loading doses of 9200 +/- 2400 mg over 10 +/- 4 days. The symptoms were palpitations (n = 2) associated in one patient with hypotension, one syncope, one near syncope and one cardiogenic shock. The ventricular cycle of the 1/1 flutter was 287 +/- 33 ms. The QRS duration was 136 +/- 35 ms with ventricular tachycardia-like appearances in 3 cases. An adrenergic trigger factor was noted in 5 patients. One patient required emergency cardioversion. The authors discuss the physiopathology of 1/1 flutter and theoretical diagnostic methods are proposed. In conclusion, amiodarone does not always prevent the occurrence of 1/1 nodo-ventricular conduction in atrial flutter.

Administration, Oral↗
PubMed2003

Enlarged effects of adenosine in a septic patient with multiple myeloma and atrial flutter.

We report the history of a 60-year-old patient with a multiple myeloma and Staphylococcus aureus associated sepsis to whom adenosine in a dose of 6 mg was administered, when a regular, narrow QRS complex tachycardia at a heart rate of 120 beats/minute started. Adenosine led to a complete AV-block and revealed atrial flutter. Atrial flutter waves persisted for about 15 seconds and were followed by atrial and ventricular asystole for about 20 seconds. Repeated nonsustained polymorphic ventricular tachycardias followed and after about 90 seconds sinus rhythm was restored.

Adenosine↗
PubMed1989

Electrophysiologic basis of catheter ablation in atrial flutter.

A reentrant mechanism is believed to be responsible for atrial flutter. The recent development of the entrainment criteria further supports this theory, and there is a general consensus that circus movement is the underlying abnormality that supports this arrhythmia. In most clinical studies, abnormal fragmented (or double spike) electrograms, suggesting the presence of areas of localized slowing of conduction or block, have been reported. They are almost always recorded in the lower and posterior portion of the right interatrial septum, but also frequently in the high lateral portion of the right atrium. The determination of their involvement in the reentry pathway is important for designing curative procedures such as surgery or ablation. The low atrial septal area surrounding the mouth of the coronary sinus was suspected as being the critical area of slow conduction in atrial flutter. Rapid pacing at that site can yield a surface electrocardiographic pattern similar to the clinically occurring arrhythmias. Additionally, the flutter circuit can be accelerated during atrial pacing at fixed and slightly faster rates than the intrinsic tachycardia rate--the so-called entrainment phenomenon. When entrainment criteria are fulfilled, tachycardia termination being by definition ruled out, any concomitant recorded local type II block identifies an area that must be outside the circuit. Such local block may be recorded either spontaneously or during entrainment and therefore helps in identifying atrial slow conduction areas that do not belong to the reentrant path. This approach was applied to identify the optimal ablation site in 8 patients with long-standing drug resistant atrial flutter. In 7 of 8 patients, we were able to identify a fragmented potential in the low posteroseptal area during sustained atrial flutter.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Flutter↗
PubMed2002

Repetitive atrial flutter as a complication of the left-sided simple maze procedure.

BACKGROUND: Of 41 patients who had undergone a left-sided simple maze procedure, 4 (9.8%) developed repetitive tachycardia due to atrial flutter, and required radiofrequency catheter ablation. Linear ablation of the right atrial isthmus was effective to treat atrial flutter. METHODS: We conducted an electrophysiologic study of atrial flutter and determined its reentry circuit on the atrium. We consider how to reduce atrial flutter after the left-sided simple maze procedure. RESULTS: Common atrial flutter through the right atrial isthmus was induced in all 4 patients, and linear ablation on the right atrial isthmus was effective in 3 of these. An incisional atrial flutter around the right atriotomy was also induced in 2 of 4 patients; both were successfully treated by linear ablation between the right atriotomy and the inferior vena cava. CONCLUSIONS: Common atrial flutter through the right atrial isthmus is a risk after the left-sided simple maze procedure. When a left-sided simple maze procedure is performed, sufficient cryoablation on the right atrial isthmus of the arrested heart should be administered to prevent postoperative atrial flutter.

Adult↗
PubMed1997

Relationship between atrial fibrillation and typical atrial flutter in humans: activation sequence changes during spontaneous conversion.

BACKGROUND: A transitional rhythm precedes the spontaneous onset of atrial flutter in an animal model, but few data are available in man. METHODS AND RESULTS: In 10 patients, 16 episodes of atrial fibrillation (166+/-236 seconds) converting into atrial flutter during electrophysiological evaluation were analyzed. A 20-pole catheter was used for mapping the right atrial free wall. Preceding the conversion was a characteristic sequence of events: (1) a gradual increase in atrial fibrillation cycle length (150+/-25 ms after onset, 166+/-28 ms before conversion, P<.01); (2) an electrically silent period (267+/-45 ms); (3) "organized atrial fibrillation" (cycle length, 184+/-24 ms) with the same right atrial free wall activation direction as during atrial flutter; (4) another delay on the lateral right atrium (283+/-52 ms); and (5) typical atrial flutter (cycle length, 245+/-38 ms). The coronary sinus generally had a different rate than the right atrial free wall until the beat that initiated flutter, when right atrium and coronary sinus were activated in sequence. During 1313 seconds of fibrillation, there were 171 episodes of "organized atrial fibrillation." An additional activation delay at least 30 ms longer than the mean organized atrial fibrillation cycle length was sensitive (100%) and specific (99%) for impending organization into atrial flutter. During organized atrial fibrillation, right atrial free wall activation was craniocaudal in 70% and caudocranial in 30%, which may explain why counterclockwise flutter is a more common clinical rhythm than clockwise flutter. Atrial flutter never degenerated into fibrillation, even after adenosine infusion. CONCLUSIONS: Anatomic barriers, along with statistical properties of conduction and refractoriness during atrial fibrillation, may explain the remarkably stereotypical pattern of endocardial activation during the initiation of atrial flutter via fibrillation and the rarity of degeneration of flutter to fibrillation once it stabilizes.

Aged↗
PubMed2001

Symptomatic improvement after radiofrequency catheter ablation for typical atrial flutter.

OBJECTIVE: To assess the changes in quality of life, arrhythmia symptoms, and hospital resource utilisation following catheter ablation of typical atrial flutter. DESIGN: Patient questionnaire to compare the time interval following ablation with a similar time interval before ablation. SETTING: Tertiary referral centre. PATIENTS: 63 consecutive patients were studied. Four patients subsequently underwent an ablate and pace procedure, two died of co-morbid illnesses, and two were lost to follow up. The remaining 55 patients form the basis of the report. RESULTS: Patients were followed for a mean (SD) of 12 (9.5) months. Atrial flutter ablation resulted in an improvement in quality of life (3.8 v 2.5, p < 0.001) and reductions in symptom frequency score (2.0 v 3.5, p < 0.001) and symptom severity score (2.0 v 3.8, p < 0.001) compared with preablation values. There was a reduction in the number of patients visiting accident and emergency departments (11% v 53%, p < 0.001), requiring cardioversion (7% v 51%, p < 0.001), or being admitted to hospital for a rhythm problem (11% v 56%, p < 0.001). Subgroup analysis confirmed that patients with atrial flutter and concomitant atrial fibrillation before ablation and those with atrial flutter alone both derived significant benefit from atrial flutter ablation. Patients with concomitant atrial fibrillation had an improvement in quality of life (3.5 v 2.5, p < 0.001) and reductions in symptom frequency score (2.3 v 3.5, p < 0.001) and symptom severity score (2.2 v 3.7, p < 0.001) compared with preablation values. CONCLUSIONS: Ablation of atrial flutter is recommended both in patients with atrial flutter alone and in those with concomitant atrial fibrillation.

Adult↗
PubMed1992

Catheter ablation by low energy DC shocks for successful management of atrial flutter.

OBJECTIVE: To assess the effects of low energy ablation of the substrate for atrial flutter. DESIGN: Initial retrospective analysis of patients undergoing low energy ablation of the atrioventricular node for refractory atrial flutter (group 1) was followed by a prospective assessment of low energy ablation in the posterio-inferior right atrium for the same condition (group 2). SETTING: Tertiary referral centre for management of cardiac arrhythmias. PATIENTS: Seven men (aged 50-67 years) with refractory atrial flutter. INTERVENTIONS: Multiple (3-10) low energy DC shocks with a cumulative energy of 100-245 J in the region of the atrioventricular node in group 1 and 12-15 low energy DC shocks (cumulative energy 110-235 J) guided by the anatomical landmarks of the triangle of Koch and applied directly to the atrial wall. MAIN OUTCOME MEASURE: Freedom from recurrence of atrial flutter. RESULTS: In group 1 despite initial complete atrioventricular block in three patients, atrioventricular conduction had resumed in all by one month. All four, however, were in sinus rhythm at follow up six to 13 months later. Two of the three patients in group 2 were free of atrial flutter at follow up three to four months after ablation. CONCLUSION: Ablation of the atrial flutter substrate with low energy DC shocks is feasible. Precise electrophysiological mapping is not necessary.

Aged↗
PubMedDate not supplied

Inducible atrial flutter and fibrillation after orthotopic heart transplantation.

Inducible atrial flutter (two patients) and fibrillation (two patients) were observed in a series of 35 heart transplant patients who underwent evaluation of sinus node function including premature atrial stimulation. The sinus node function was entirely normal in both patients with inducible atrial flutter. In contrast it was profoundly abnormal in the patients with inducible atrial fibrillation. Atrial fibrillation was no longer inducible as the sinus node function became borderline normal. These observations suggest extensive electrical atrial abnormality, including the sinus node, in patients with atrial fibrillation, and temporary pacing should be available when considering cardioversion in patients with atrial fibrillation early after heart transplantation. Atrial flutter, in contrast, may be inducible in the absence of any sinus node abnormality and without any evidence of rejection.

Adult↗
PubMed1995

Mechanisms of atrial flutter: implications for ablative therapy.

Much has been learned about atrial flutter mechanisms from studies in animal models and in patients. In fact, it seems virtually always due to some form of reentry. Furthermore, it seems likely that there is more than one location of the atrial flutter reentrant circuit in patients, although the reentrant circuit in most instances of atrial flutter seems to be activation up the interatrial septum and then down the posterior right atrial free-wall. Other locations of the reentrant circuit may include the right atrial free-wall alone or the tricuspid valve annulus, among others. Resolution of this awaits better mapping data from human studies. Clearly, an understanding of mechanism is central to achieving effective ablation. Thus, if it is possible to identify a critical aspect or aspects of the atrial flutter mechanism vulnerable to therapy with ablative energy, effective treatment using ablative techniques should be successful.

Atrial Flutter↗