Atrial Flutter Patients Research Articles

Four types of outcomes after right atrial isthmus ablation of atrial flutter in patients with atrial flutter and fibrillation

Four types of outcomes after right atrial isthmus ablation of atrial flutter in patients with atrial flutter and fibrillation

Four types of outcomes after right atrial isthmus ablation of atrial flutter in patients with atrial flutter and fibrillation

Four types of outcomes after right atrial isthmus ablation of atrial flutter in patients with atrial flutter and fibrillation

Electrophysiological characteristics and radiofrequency ablation of focal atrial tachycardia originating from the superior vena cava.

The initiation of focal atrial tachycardia (AT) from the superior vena cava (SVC) remains unclear. In 3 patients (2 females, 1 male; aged 57, 66 and 50 years, respectively) with focal AT arising from different parts of the SVC, the AT occurred spontaneously, rather than being induced by electrical stimulation. The cycle length of the tachycardia was highly variable, ranging between 190 and 300 ms in patient 1, 180 and 320ms in patient 2, and 200 and 300ms in patient 3. The clinical or associated arrhythmias were atrial fibrillation (AF) (patients 1, 3) and atrial flutter (AFL) (patients 2, 3). A presumed SVC potential that was earlier than the activation of all the other mapping sites was recorded during AT at the lower anterior (15-mm above the atriocaval junction), the mid-anterior (25-mm above the atriocaval junction) and the lower posterior aspect of the SVC (17-mm above the atriocaval junction. Radiofrequency (RF) ablation targeting the SVC focus with the SVC potential promptly eliminated the focal AT in all 3 patients. The coexistent typical AFL was ablated, but the AF was not. The follow-up period was 6, 6, and 3 months, respectively, for each of the patients under no antiarrhythmic medication; there has not been a recurrence of symptomatic palpitation. In conclusion, focal electrical firing in the SVC can initiate AT and this type of focal AT is always associated with AFL or AF. RF ablation guided by the presumed SVC potential is safe and highly effective in eliminating the tachycardia.

Dofetilide: A new antiarrhythmic agent approved for conversion and/or maintenance of atrial fibrillation/atrial flutter.

Dofetilide is a new antiarrhythmic agent recently approved for the conversion of and maintenance of sinus rhythm in patients with atrial fibrillation (AF) and atrial flutter (AFl). Dofetilide is a selective class III antiarrhythmic drug which works by selectively blocking the rapid component of the delayed rectifier outward potassium current (I(kr)). Dofetilide has been shown to prolong the effective refractory period which is accompanied by a dose-dependent prolongation of the QT and QTc intervals, with parallel increases in ventricular refractoriness. Approximately 80% of dofetilide is excreted in the urine which requires dose adjustments in renal insufficiency. The elimination half-life is approximately 10 h in patients with normal renal function. The therapeutic blood level range of dofetilide is presently unknown and monitoring of dofetilide blood levels is not available at this time. Clinical trials have shown dofetilide to be superior to flecainide in converting AFl patients to normal sinus rhythm (NSR) (70% vs. 9%; p<0.01). It also was more effective than sotalol in converting AF and AFl patients to NSR (29% vs. 6%; p<0.05) and maintaining these patients in NSR for up to 1 year (p<0.05). Most patients convert to NSR within 24-36 h. Torsade de pointes is the most serious side effect occurring in 0.3-10.5% of patients and is dose related. Other common side effects include headache, chest pain and dizziness. To minimize the risk of induced arrhythmia, patients initiated or reinitiated on dofetilide should be hospitalized for a minimum of 3 days where continuous electrocardiographic monitoring, evaluation of renal function and serum electrolytes and cardiac resuscitation can be provided.

Incidence and clinical significance of transformation of atrial fibrillation to atrial flutter in patients undergoing long-term antiarrhythmic drug treatment.

To investigate the rate of transformation of atrial fibrillation to atrial flutter in patients taking antiarrhythmic drugs for the prophylaxis of atrial fibrillation, we retrospectively analysed data from 305 consecutive patients with paroxysmal atrial fibrillation (155 male; mean age 63 +/- 11 years) treated with ventricular rate controlling drugs, antiarrhythmic drugs, or without drugs. At a mean follow-up of 9 months (range 1-24) all patients experienced recurrence of arrhythmia: 48 (14.6%, Group A) suffered Type 1 atrial flutter, and 257 (85.4%, Group B) atrial fibrillation. The relative rate of recurrence of atrial flutter vs atrial fibrillation was similar in patients without treatment or with ventricular rate controlling drugs (from 6.8% to 14.6%, P=ns). However, recurrence was higher (25%) in patients administered antiarrhythmic drug therapy. The relative risk in these patients was 3.02 times greater, compared with patients without treatment, or treated with rate controlling drugs (P<0.001). There were no differences between groups concerning the baseline clinical characteristics and the clinical consequences of the recurrence; patients with atrial flutter had a lower rate of conversion to sinus rhythm (42% vs 64%) and a higher rate of hospital admission (69% vs 36%) compared with those with atrial fibrillation. Six patients (8.5%) experienced 1:1 atrioventricular conduction during atrial flutter with a ventricular rate of 240-280 beats x min(-1). Our data suggest that the use of antiarrhythmic drugs for the prophylaxis of atrial fibrillation is associated with a threefold increase in the probability of Type 1 atrial flutter recurrence, as opposed to atrial fibrillation, which may have important clinical consequences, but which did not in our study.

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

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

What is the relationship of atrial flutter and fibrillation?

Animal models and human studies of atrial activation mapping and entrainment have considerably enhanced our understanding of the anatomical substrate for atrial flutter and created the basis for a definite cure with radiofrequency catheter ablation. As atrial flutter has now become a curable arrhythmia, emphasis is shifting to understand the most common arrhythmia: atrial fibrillation. Furthermore, from clinical observation, it is apparent that there is a relationship between atrial fibrillation and atrial flutter in patients with atrial arrhythmias. Techniques that have informed our understanding of the anatomical basis of atrial flutter may also be useful in understanding the relationship between atrial fibrillation and flutter, including animal models, clinical endocardial mapping, and intracardiac anatomical imaging. Thus, atrial anatomy and its relationship to electrophysiological findings, and the role of partial or complete conduction barriers around which reentry can and cannot occur, may be of importance for atrial fibrillation as well. Ultimately, the relationship between atrial fibrillation and atrial flutter may inform our understanding of the mechanisms of atrial fibrillation itself, and help to develop new approaches to device, catheter-based, and pharmacological therapy for atrial fibrillation.

Anticoagulation for cardioversion of atrial arrhythmias.

We would advocate 3 weeks of anticoagulation prior to, and 4 weeks post-cardioversion (either electrical or chemical) for patients in chronic atrial fibrillation or flutter. In selected cases it seems reasonable to use transoesophageal echocardiography to exclude preformed thrombus and negate the need for 3 weeks of prior anticoagulation. For patients presenting acutely with atrial fibrillation or flutter we suggest anticoagulating with heparin immediately on presentation and for those who do not spontaneously revert to sinus rhythm, using transoesophageal echocardiography to exclude atrial thrombi prior to cardioversion. Oral anticoagulation should be continued for 4 weeks post-procedure. If transoesophageal echocardiography is not readily available an alternative strategy would be to anticoagulate the patient for 3 weeks and thereafter readmit them for elective cardioversion, continuing the anticoagulation for a further 4 weeks after the procedure.

A canine model of atrial flutter following the intra-atrial lateral tunnel fontan operation

Atrial flutter (AFL) is a common problem in children who have undergone a Fontan operation for single ventricle physiology. Although this has been attributed to the atrial stretch inherent in the earlier forms of this operation, AFL has persisted in spite of a modification that minimizes atrial distension. Therefore, it was hypothesized that AFL following the modified Fontan procedure may result from anatomic barriers related to suture lines rather than from atrial stretch or hypertension. In a series of experiments performed in dogs under general anesthesia, the modified Fontan repair was simulated by placing only the suture line of the intra-atrial repair. No baffle was placed, thus avoiding any hemodynamic alterations. After closure of the atriotomy, 253 point unipolar atrial endocardial form-fitting electrodes were inserted through the mitral and tricuspid valves via bilateral ventriculotomies. Induction of AFL was attempted with atrial burst pacing and programmed extrastimulation, and activation sequence maps of subsequent reentry were generated from the endocardial electrodes. Atrial flutter was induced in all of 17 dogs, with a median cycle length of 177 ± 31 ms. Activation sequence maps demonstrated conduction block along the crista terminalis corresponding to the free wall portion of the suture line. This created an isthmus between the suture line and tricuspid annulus, which appeared critical for sustaining AFL, although the circuit used both the septal and free wall surfaces of the right atrium. In seven dogs, a cryolesion was placed from the tricuspid annulus to the free wall segment of the suture line, terminating the AFL, in all seven. When the free wall segment of the suture line was moved 5 mm medial to the crista terminalis, AFL was induced in four of five dogs, but only in the presence of isoproterenol and at a shorter cycle length (136 ± 8 ms, P < .001). Atrial flutter was not inducible, even with the addition of isoproterenol, in any of five dogs in which the suture line was placed 10 mm anterior to the crista terminalis and incorporated into closure of the atriotomy. This acute canine model of the modified Fontan operation demonstrates that conduction block from the free wall portion of the suture line creates an isthmus of tissue between the suture line and the tricuspid annulus. This is a sufficient substrate to produce AFL; no hemodynamic alteration is required. Injury to the crista terminalis is a significant risk factor in this model, which suggests that a modification of the suture line might reduce the incidence of AFL in patients following this operation.

Electrical Remodeling of the Human Atrium: Similar Effects in Patients With Chronic Atrial Fibrillation and Atrial Flutter

Objectives. This study sought to determine whether chronic atrial fibrillation (AF) and atrial flutter in patients lead to electrical remodeling of the human atrial myocardium, manifested by an abnormal relation between atrial cycle length and action potential duration (APD).Background. Experimental studies in goats and isolated human atrial tissue have shown that prolonged AF leads to persistent shortening of atrial refractoriness, a phenomenon referred to as electrical remodeling and which helps to explain why AF begets AF. Direct data on human in situ myocardium are still lacking.Methods. Using monophasic action potential recordings at two right atrial sites simultaneously, we determined in 7 patients with chronic AF and 13 with chronic atrial flutter (3 weeks to 3 years in duration) the relation between paced cycle length and APD at 90% repolarization (APD90) 15 to 30 min after conversion to sinus rhythm. APD90 was measured during regularly paced cycle lengths (250 to 800 ms) to determine the steady state cycle length relation and during extrastimulus intervals (from 800 ms to refractoriness) at a basic cycle length of 600 ms to determine electrical restitution curves. The same pacing protocols and measurements were performed in nine control patients with sinus rhythm and no overt atrial disease.Results. In control patients, steady state APD90 increased steadily with increases in cycle length from 250 to 800 ms, reaching a maximal value of 325 ± 41 ms (mean ± SD) at a cycle length of 800 ms. In patients with cardioversion from atrial flutter or AF, the steady state cycle length–APD90 relation was shifted downward and flattened at cycle lengths >400 ms, reaching only 219 ± 44 and 245 ± 39 ms, respectively, at the 800-ms cycle length (p < 0.005 vs. control). The early time course of electrical restitution (200- to 300-ms extrastimulus intervals) was similar between all three groups, but at extrastimulus intervals >350 ms, APD90 was shorter in both the AF and atrial flutter groups than in the control group (p < 0.05). There were no significant differences between patients with cardioversion from atrial flutter and those with cardioversion from AF. APD90 at a steady state cycle length of 600 ms showed no significant correlation with the duration of previous AF or atrial flutter.Conclusions. AF and atrial flutter lead to marked, quantitatively similar decreases in the right atrial APD during steady state pacing and extrastimulation a considerable time after cardioversion. These data confirm that both AF and atrial flutter lead to electrical remodeling in the human atrium, with a preponderance at longer cycle lengths. It may be prudent to abort both types of arrhythmias early to prevent electrical remodeling.

Factors that influence the development of atrial flutter after the fontan operation

Objectives: Atrial flutter is a frequent, potentially fatal complication of the Fontan operation, but risk factors for its development are ill defined. We evaluated clinical features that might predict the development of atrial flutter in patients who had a Fontan operation. Methods: We evaluated 334 early survivors of a Fontan operation done between April 1973 and July 1991 (mean follow-up, 5.0 ± 3.8 years). Evaluation included electrocardiography, Holter monitor recordings, and chart review. Modifications of the Fontan operation included an extracardiac conduit ( n = 43), an atriopulmonary anastomosis ( n = 117), or a total cavopulmonary anastomosis ( n = 174). Patient, time, and procedure-related variables were analyzed with respect to the development of atrial flutter. Results: Atrial flutter was identified in 54 (16%) patients at a mean of 5.3 ± 4.7 years (range 0 to 19.7 years) after Fontan operation. Atrial flutter developed sooner and was more likely to occur in patients who were older at the time of Fontan operation (12.4 ± 7.6 vs 6.3 ± 5.2 years; p < 0.001), had a longer follow-up interval (8.7 ± 3.9 vs 4.4 ± 3.4 years; p < 0.001), had a prior atrial septectomy or pulmonary artery reconstruction ( p < 0.01), and had worse New York Heart Association class symptoms ( p < 0.02). The presence of sinus node dysfunction was associated with a higher incidence of atrial flutter ( p < 0.001). Although there was a lower prevalence of atrial flutter in those patients with a total cavopulmonary anastomosis, the follow-up for this group was shorter. Anatomic diagnoses, perioperative hemodynamics, and other previous palliative operations were not associated with an increased incidence of atrial flutter. Multivariate analysis identified age at operation, duration of follow-up, extensive atrial baffling, and type of repair as factors associated with the development of atrial flutter after Fontan operation. Conclusion: Atrial flutter continues to develop with time after the Fontan operation. Further follow-up is necessary to determine whether a total cavopulmonary anastomosis reduces the incidence of atrial flutter. (J Thorac Cardiovasc Surg 1997;113:80-6)

Spontaneous Onset of Type I Atrial Flutter in Patients

Spontaneous Onset of Type I Atrial Flutter in Patients

Spontaneous onset of type I atrial flutter in patients

Objectives. This study sought to characterize the spontaneous onset of atrial flutter in patients.Background. Temporary epicardial electrodes are routinely placed on the atria of patients at the time of open heart surgery and brought out through the anterior chest wall for potential diagnostic and therapeutic use in the postoperative period. We utilized these electrodes to study the spontaneous onset of type I atrial flutter in 16 patients in the postoperative period after open heart surgery.Methods. Twenty-seven episodes of the spontaneous onset of type I atrial flutter from sinus rhythm were studied in these 16 patients by recording bipolar atrial electrograms simultaneously with at least one electrocardiographic lead during each episode.Results. In all 27 episodes, the onset of type I atrial flutter was through a transitional rhythm of variable duration (mean 9.3 s) precipitated by a premature atrial beat. In 21 episodes, the transitional rhythm was atrial fibrillation; in 3 episodes it was type II atrial flutter that appeared to generate atrial fibrillation; and in 3 episodes it was a brief (3 to 6 beats), rapid, irregular arrhythmia.Conclusions. Type I atrial flutter does not start immediately after a premature atrial beat. Rather, it starts after a transitional rhythm that is usually atrial fibrillation. Extrapolating from mapping studies of the onset of atrial flutter in the canine pericarditis model, we suggest that a transitional rhythm is required for the initiation of type I atrial flutter because during that rhythm, the requisites for development of the atrial flutter reentry circuit evolve.

Characterization and surgical ablation of atrial flutter after the classic fontan repair

Atrial flutter (AFL) is a frequent postoperative complication of the classic Fontan operation, which uses an atriopulmonary connection. We hypothesized that the suture lines alone, in the absence of any hemodynamic alterations, provide the necessary electrophysiologic substrates for AFL. The objectives of this study were to determine if the Fontan suture lines alone are sufficient to permit sustained AFL in an acute canine model and to characterize any resulting reentrant circuits to surgically ablate the AFL. After cardiopulmonary bypass, adult dogs (n = 18) underwent a simulated classic Fontan operation. This included a longitudinal right atriotomy and an incision from the base of the right atrial appendage toward the dome of the left atrium, representing the atriopulmonary connection. In 6 of 18 dogs, an atrial septal defect was created at the level of the fossa ovalis. Unipolar 253-point biatrial endocardial mapping electrodes were placed via bilateral ventriculotomies. Induction of AFL was attempted by atrial burst pacing. If AFL could not be induced, isoproterenol was administered and pacing repeated. Activation sequence maps of the pathways of atrial reentry were generated. In 8 dogs with inducible AFL, an incision was made from the atriotomy to the atriopulmonary connection and burst pacing repeated. Sustained AFL could not be induced after bypass alone in any case. After the simulated Fontan operation, sustained AFL was reproducibly induced in all 18 dogs, 6 of which required isoproterenol. The mean cycle length of all cases was 177 +/- 20 ms. During AFL, atrial activation sequence maps demonstrated lines of conduction block created by both the atriotomy and the atriopulmonary connection. The isthmus of tissue between these two lines of block was essential for propagation of the reentrant wavefront. Interruption of this isthmus with an incision successfully terminated AFL in 8 of 8 dogs. In an acute canine model, the Fontan suture lines alone, in the absence of atrial hypertension or stretch, permit the induction of AFL. An essential electrophysiologic substrate is an isthmus of myocardium between the atriotomy and the atriopulmonary connection. Interruption of conduction through this isthmus terminates the AFL in this model and suggests a technique for ablation of AFL in patients who have undergone a classic Fontan operation.

Radiofrequency ablation of intra-atrial reentrant tachycardia after surgical palliation of congenital heart disease.

Intra-atrial reentrant tachycardia (IART), also called atrial flutter, is a common and potentially lethal complication of surgical correction of congenital heart disease. Medical management of IART is often problematic, which prompts an investigation of the utility of radiofrequency (RF) ablation for management of these arrhythmias. Ten consecutive patients referred for treatment of recurrent IART after surgery for congenital heart disease were studied. Median age was 18.4 years, and median duration of arrhythmia was 6.4 years; a median of three antiarrhythmic drugs had been tried. Surgical procedures used were Fontan (6), Mustard/Senning (2), and biventricular repair (2). Intracardiac electrophysiological study demonstrated 30 distinct IART circuits, defined by activation sequence and cycle length. Mean IART cycle length was 323 +/- 114 ms. Cycle length was significantly longer in IART circuits that were successfully ablated compared with those that were not (381 versus 248 ms, P < .001). RF ablation was attempted in 22 of these circuits. Ablation sites were targeted to presumed exit points from zones of slow conduction by electrophysiological criteria. Sites chosen in this manner clustered in four distinct areas of the right atrium. Of 22 IART circuit ablations attempted, 17 (77%) resulted in acute termination of the tachycardia. In 8 of 10 patients in whom at least one IART circuit was successfully ablated, 4 are free of clinical tachycardia and 3 are improved over short-term follow-up. No complications were encountered. Multiple IART circuits may be present in patients after surgery for congenital heart defects. Activation sequences observed were diverse and different from those observed in atrial flutter in patients with normal anatomy. Interruption of IART circuits by RF ablation is feasible using mapping techniques aimed at identifying an exit point from a zone of slow conduction. Short-term follow-up suggests that RF ablation may be a useful adjunct in management of IART in these difficult patients.

943-10 Excellent Long-term Outcome of DC Electrical Cardioversion in Patients with Atrial Flutter

The aim of the present study was to investigate long-term outcome in patients with chronic atrial flutter (AFL) who underwent at least one DC electrical cardioversion (ECV) and who were treated with an intention-to-maintain sinus rhythm (SR). Included were 83 patients, 37% suffered from coronary artery disease, 27% from valvular disease, 20% from congenital heart disease, 6% from hypertension, and 10% had ‘lone’ AFL. Mean age was 55 ± 15 years. Median previous arrhythmia history was 3 months. Mean echocardiographic long axis left atrial size was 45 ± 9 mm. ECV was successful in 81 patients (99%). After AFL recurrence prophylactic antiarrhythmic drugs were instituted after re-ECV according to a stepped care approach, first sotalol followed by a Class IC and as last resort amiodarone. Mean follow-up was 4 ± 1 years. Life table analysis showed that after 2 years 50% of the patients were in SR after 1 ECV (figure). After 2 ± 1 ECVs 82% was in SR at the end of follow-up. Multivariate analysis revealed that the only parameter related to maintenance of SR was the left ventricular end-systolic diameter (p = 0.03). patients with AFL show excellent long-term maintenance of SR. These data indicate that ECV is the therapy of choice in AFL patients. RF ablation of AFL should be kept as last resort therapy.

Association between atrioventricular node reentrant tachycardia and inducible atrial flutter

Objectives. The purpose of this study was to evaluate the inducibility of atrial flutter in patients with atrioventricular (AV) node reentrant tachycardia and to determine the effect of radio-frequency ablation of the slow AV node pathway on the inducibility of atrial flutter.Background. Studies have shown that both AV node reentrant tachycardia and atrial flutter are reentrant arrhythmias having an area of slow conduction that is located in the low posterior right atrium near the ostium of the coronary sinus.Methods. Ninety-one patients were prospectively evaluated using a standardized atrial pacing protocol. Three groups of patients were analyzed: 42 patients with inducible AV node reentrant tachycardia, 13 with a history of spontaneous atrial flutter and 36 control patients. A subgroup of 34 patients with AV node reentrant tachycardia who underwent successful radiofrequency ablation of the slow AV node pathway underwent atrial pacing again after ablation.Results. Atrial flutter was more frequently inducible in patients with AV node reentrant tachycardia (88%) and in those with a history of atrial flutter (92%) than in control patients (36%) (p = 0.0001). There were no differences between the patient groups with respect to atrial effective refractory period, P wave duration or PA interval at the His position. Among the 34 patients with AV node reentrant tachycardia who underwent atriai pacing before and after radiofrequency ablation, there were 30 with atrial flutter and 4 with atriail fibrillation before ablation and 29 with atrial flutter and 5 with atrial fibrillation after ablation (p = NS). There was no difference in the duration of the induced atrial flutter before and after ablation. The mean atrial flutter cycle length before ablation (206 ± 22 ms) was not different from that after ablation (196 ± 20 ms) (p = NS).Conclusions. There is a strong association between AV node reentrant tachycardia and inducible atrial flutter, suggesting that there may be a common area of perinodal atrium participating in the two tachycardia circuits. However, radiofrequency ablation of the slow pathway of the AV node reentrant tachycardia circuit does not influence the inducibility of atrial flutter.

Successful intracardiac electrical conversion of atrial flutter in patients with complex congenital heart disease.

Sixteen patients presenting on 21 occasions with atrial flutter in association with complex congenital heart disease were treated by intracardiac stimulation techniques combined with activation mapping. Nineteen episodes of atrial flutter were successfully converted to sinus rhythm. In the remaining two episodes atrial fibrillation was induced with spontaneous conversion to sinus rhythm within 12 hours in one episode and immediate DC cardioversion to sinus rhythm in the other. Intracardiac stimulation techniques were highly successful in this group and allowed reliable conversion to sinus rhythm without general anaesthesia and high energy cardioversion. In patients with atrial flutter associated with congenital heart disease intracardiac stimulation techniques should be tried first.

Atrial flutter in patients treated for atrial fibrillation with propafenone

The class IC antiarrhythmic drug, propafenone, has been used successfully for the prevention of atrial fibrillation (AF), with few reported adverse cardiovascular effects. 1–3 Propafenone depresses the rate of rise and amplitude of phase 0 of the action potential, slowing conduction in the atrium. 4 Although it has mild β-adrenergic antagonist effects, it has relatively less effect on atrioventricular refractoriness, although in AF the ventricular response may slow. 5 With slower atrial arrhythmias such as atrial flutter, where less concealment of conduction occurs, it is possible that the same effect on ventricular rate may not be seen. This study defines the incidence of atrial flutter developing in a heterogeneous population of patients with recurrent AF and observes the ventricular response during this arrhythmia.

Facilitating influence of disopyramide on atrial flutter termination by overdrive pacing

Long-lasting (mean 30 days) type I atrial flutter was treated with overdrive pacing in 30 patients (mean age 69 years) with organic heart disease. To evaluate the effect of pretreatment with disopyramide, the study population was divided in 3 groups of 10 patients each: group A, no disopyramide therapy; group B, intravenous disopyramide (maximum dose 250 mg in 1 hour); and group C, oral disopyramide (400 mg daily for 4 days). There were no differences in baseline cycle length of atrial flutter among the 3 groups before drugs were given. The stimulation protocol included overdrive atrial pacing up to the shortest paced cycle of 150 ms performed at a maximum of 3 atrial sites. Reversion to sinus rhythm occurred in 2 patients in group A, 7 in group B (p < 0.01) and 5 in group C. Pacing was performed from a mean number of 2.1 sites/patient in group A, 1.2 in group B and 2.0 in group C. Atrial fibrillation occurred in 7, 3 and 4 patients, respectively. Acceleration to a faster form of atrial flutter occurred in 3, 3 and 4 patients, respectively, and reversion to sinus rhythm occurred in all patients who had intravenous disopyramide and in 1 who took the drug orally. The administration of disopyramide before overdrive pacing improved the rate of conversion to sinus rhythm and allowed an easier stimulation protocol with a lower incidence of pacing-induced atrial fibrillation. Disopyramide is beneficial when overdrive atrial pacing is performed for the treatment of long-standing atrial flutter in patients with organic heart disease.