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PubMed1990

Characterization of double potentials in human atrial flutter: studies during transient entrainment.

Double potentials, defined as atrial electrograms with two discrete deflections per beat separated by an isoelectric interval or a low amplitude baseline, have been observed during right atrial endocardial mapping of human atrial flutter. In this study, bipolar atrial electrograms were recorded during atrial flutter (mean cycle length 235 +/- 27 ms [+/- SEM]) from the high right atrium, the His bundle region, the coronary sinus and at least 30 right atrial endocardial mapping sites in 10 patients. Double potentials were recorded from the right atrium in all patients during atrial flutter. Double potentials were evaluated during transient entrainment of atrial flutter by rapid high right atrial pacing in 5 of the 10 patients. In four of these five patients during such transient entrainment 1) one deflection of the double potential was captured with a relatively short activation time (mean interval 89 +/- 45 ms) and the other deflection was captured with a relatively long activation time (mean interval 233 +/- 24 ms), producing a paradoxical decrease in the short interdeflection interval from a mean of 75 +/- 20 ms to a mean of 59 +/- 24 ms; and 2) the configuration of the double potential remained similar to that observed during spontaneous atrial flutter. On pacing termination 1) the two double potential deflections were found to be associated with two different atrial flutter complexes in the electrocardiogram (ECG); 2) the previous double potential deflection relation resumed; and 3) when sinus rhythm was present, the double potentials were replaced by a broad, low amplitude electrogram recording at the same site.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

Paroxysmal atrial flutter caused by cardiac lymphoma.

Atrial flutter is a relatively frequent macro-reentrant tachycardia that can be caused by a variety of structural and functional atrial changes. Cardiac lymphoma is rare and usually carries a poor prognosis. It preferentially involves the right atrium. This report describes a patient with cardiac follicular B-cell lymphoma who developed paroxysmal atrial flutter. The large tumor mass created a macroscopic substrate for an area of slow conduction which is essential for atrial flutter. It also caused sinus arrest and intermittent obstruction of the tricuspid valve inlet.

Aged↗
PubMed1998

Atrial flutter in the neonate and early infancy.

Atrial flutter is a rare arrhythmia in the neonate and early infancy. We retrospectively reviewed the clinical presentations, treatment and outcome of seven patients who presented clinically with atrial flutter. The age of onset ranged from 1 day to 3 months. Atrial flutter was diagnosed in the first 3 days of life in 4. Three cases presented as atrial flutter with 2:1 atrioventricular conduction and the remaining 4 with variable AV block. Heart failure was present in 3 patients and 6 patients showed normal intracardiac structure on echocardiography. Electrical cardioversion was attempted as the first treatment in 4 cases, followed by digoxin in three of the four. Digoxin was given as an initial therapy in 2 patients. One patient recovered spontaneously without treatment. In the 6 patients who received therapy, 5 converted to normal sinus rhythm within 2 days. The remaining patient had ventricular ectopic beats for about 4 months. Only 2 cases were maintained on oral digoxin for at least 4 months after discharge. No patient had a recurrence of atrial flutter during the follow-up period which ranged from 6 months to 7 years. We conclude that there is a good long-term prognosis for atrial flutter in the neonate. Digoxin and DC cardioversion may be effective as initial therapy. Long-term digoxin prophylaxis after conversion to sinus rhythm may be not necessary.

Age of Onset↗
PubMed1997

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.

Action Potentials↗
PubMed1998

Long-term outcome of radiofrequency catheter ablation for typical atrial flutter: risk prediction of recurrent arrhythmias.

INTRODUCTION: Little is known about the predictors of recurrent atrial flutter or fibrillation after successful radiofrequency ablation of typical atrial flutter. In addition, there is only limited evidence suggesting that elimination of atrial flutter would modify the natural history of atrial fibrillation in patients who experienced both of these arrhythmias. The aims of the present study were to investigate the long-term results of radiofrequency catheter ablation and to examine the predictors for late occurrence of atrial fibrillation in a large population with typical atrial flutter. METHODS AND RESULTS: The study population consisted of 144 patients (mean age 56 +/- 18 years) with successful ablation of clinically documented typical atrial flutter. In the first 50 patients, successful ablation was defined as termination and noninducibility of atrial flutter; for the subsequent 94 patients, successful ablation was defined as achievement of bidirectional isthmus conduction block and no induction of atrial flutter. The clinical and echocardiographic variables were analyzed in relation to the late occurrence of atrial flutter or fibrillation. Over the follow-up period of 17 +/- 13 months, 14 (9.7%) patients had recurrence of typical atrial flutter. In the first 50 patients, 8 (16%) had recurrence of atrial flutter, compared with only 6 (6%) of the following 94 patients. Patients with incomplete isthmus block had a significantly higher incidence of recurrent atrial flutter than those with complete isthmus block (6/16 vs 0/78, P < 0.0001) in the following 94 patients. There was no predictor for recurrence of atrial flutter after successful ablation as determined by univariate and multivariate analysis. Although successful ablation of atrial flutter eliminated atrial fibrillation in 45% of patients with a prior history of atrial fibrillation, 31 (21.5%) of 144 patients undergoing this procedure developed atrial fibrillation during the follow-up period. Univariate analysis revealed that three clinical variables were related to the occurrence of atrial fibrillation: (1) the presence of structural heart disease; (2) a history of atrial fibrillation before ablation; and (3) inducible sustained atrial fibrillation after ablation. By multivariate analysis, only a history of atrial fibrillation and inducible sustained atrial fibrillation could predict the late development of atrial fibrillation after atrial flutter ablation. CONCLUSION: Radiofrequency catheter ablation of typical atrial flutter is highly effective and associated with a low recurrence rate of atrial flutter, but atrial fibrillation continues to be a long-term risk for patients undergoing this procedure. The presence of structural heart disease and prior spontaneous or inducible sustained atrial fibrillation increases the risk of developing atrial fibrillation.

Aged↗
PubMed2001

Disturbed atrioventricular electromechanical function long after Mustard operation for transposition of great arteries: a potential contributing factor to atrial flutter.

OBJECTIVE: The objectives were to study atrial and ventricular electromechanical function in patients long after Mustard repair for transposition of great arteries and to identify possible causes and physiologic disturbances in those with recurrent atrial flutter. METHODS: Electromechanical atrial and ventricular function was assessed in 22 patients (11 women) aged 27 +/- 5 years, 10 to 29 (mean 24) years after initial Mustard operation with electrocardiography and echocardiography. The study subjects involved 12 patients with documented atrial flutter and the remaining 10 without history of atrial arrhythmia served as controls. All patients were studied while in sinus rhythm. RESULTS: There was no difference in age, gender, or age at original Mustard surgery between the 2 patient groups. The P wave and QRS duration were significantly broader in patients compared with controls (128 +/- 14 ms vs 100 +/- 10 ms, P <.05 and 120 +/- 20 ms vs 93 +/- 6 ms, P <.01). Right ventricular end diastolic dimension was not different, whereas left ventricular fraction shortening was less (20% +/- 10% vs 35% +/- 12%, P <.01) in the patient group. Left and septal total ventricular long axes amplitude were significantly lower in patients compared with controls (1.4 +/- 0.4 cm vs 1.7 +/- 0.3 cm, P <.05 and 0.6 +/- 0.2 cm vs 1.0 +/- 0.3 cm, P <.01). Right-sided total long axis excursion was equally reduced in the 2 groups (1.0 +/- 0.3 cm). Septal and right-sided but not left-sided "a" wave was smaller in the patients (1.2 +/- 1 mm vs 3 +/- 1.2 mm, P <.001 and 1 +/- 1.3 mm vs 3 +/- 0.9 mm, P <.01). Right atrial electromechanical delay was significantly longer in patients with respect to controls (110 +/- 14 ms vs 84 +/- 25 ms, P <.001), but on the left there was no difference. The P wave duration correlated closely with right atrial electromechanical delay, r = 0.79, P <.003. Significant tricuspid regurgitation was found in 9 of 12 patients but none of the controls. CONCLUSION: Right ventricular dysfunction is present long after Mustard operation for transposition of great arteries whether flutter occurs. However, in patients with history of atrial flutter, evidence of left ventricular dysfunction, significant tricuspid regurgitation, impaired right atrial electrical and mechanical function, and reversed onset of atrial systole is also present. The consistent association of the disturbed atrial and ventricular electromechanical behavior suggests a multifactorial etiology for atrial arrhythmia.

Adult↗
PubMed2004

[Typical and atypical atrial flutters].

Definitions, classification, surface electrocardiographic characterisitics, risk for stroke and treatments. Atrial flutters are macro-reentrant circuits originated from both right and left atria. They have been classified in typical and atypical based on their cavo-tricuspid isthmus-dependence. Typical atrial flutter comprises counterclockwise and clockwise isthmus-dependent atrial flutter located within the right atrium. Atypical atrial flutters are composed by non-isthmus-dependent right atrial flutter and left atrial flutter. Typical atrial flutter represents at least 90% of all flutters, and has usually a counterclockwise pattern. Ablation is a potential definitive therapy for atrial flutter. However, successful procedures as well as complications rates are different depending of the location of the circuit. There are now evidences for risk of stroke related to atrial flutter, although epidemiological studies have not been conducted yet. Therefore, prevention of such complications using anti-thrombotic should be performed as done for atrial fibrillation.

Atrial Flutter↗
PubMed1994

Relation between cycle length, volume, and pressure in type I atrial flutter.

Assuming that type I atrial flutter is a macroreentrant circuit, its cycle length should vary with the atrial dimensions. In order to test this hypothesis, flutter cycle length was measured while inducing atrial volume and pressure changes by postural and pharmacological means in seven patients undergoing a therapeutic programmed stimulation for type I atrial flutter conversion. Right atrial volume was estimated from B-mode echocardiography data. Basal values were compared with those obtained during inspiration, expiration, Valsalva maneuver, negative tilt (head down), and positive tilt (head up) with 0.8-1.6 mg p.o. nitroglycerin. The right atrial size increased slightly from 17.8 to 18.3 cm2 (P = 0.04) during the pressure load induced by negative tilt (+3 mmHg), with a corresponding lengthening of the flutter cycle length from 228 to 233 msec (P = 0.02). Similarly, pressure unloading of -2 mmHg by positive tilting and nitrates was accompanied by a decrease in right atrial size to 16.6 cm2 (P = 0.04), with a corresponding decrease in cycle length from 228 to 219 msec (P = 0.03). Respiratory maneuver yielded similar results with an inspiratory cycle lengthening, expiratory shortening, and further shortening during Valsalva maneuver. These experiments demonstrate a direct relation between cycle length and atrial volume in human type I atrial flutter. They underline the importance of the right heart preload and atrial size for the electrophysiological characteristics of type I atrial flutter. Beside its fundamental interest, this finding is important for the understanding of the mechanism of maintenance and therapeutic responses of this common arrhythmia.

Atrial Flutter↗
PubMed2004

Clinical significance of inducible atrial flutter during pulmonary vein isolation in patients with atrial fibrillation.

OBJECTIVES: This study was designed to determine the prevalence and clinical significance of atrial flutter (AFL) that occurs during catheter ablation for atrial fibrillation (AF). BACKGROUND: Atrial flutter frequently occurs in patients with AF. METHODS: Pulmonary vein isolation was performed in 133 consecutive patients (age 52 +/- 11 years) for paroxysmal (n = 112) or persistent (n = 21) AF. A clinical episode of AFL was documented in 40 of the 133 patients (30%). During the ablation procedure, AFL occurred in 86 patients (65%), either spontaneously (n = 36) or by rapid atrial pacing (n = 50), with AFL being typical in the majority (80%). Cavo-tricuspid isthmus ablation was performed in 28 of the 133 patients. RESULTS: Among the 105 patients who did not undergo isthmus ablation, 25 patients (24%) were documented to have symptomatic AFL during a mean follow-up of 609 +/- 252 days. Among the clinical variables of age, gender, history of clinical AFL, ejection fraction, left atrial diameter, duration of AF, and occurrence of AFL during ablation, only a history of clinical AFL (p = 0.05) and occurrence of typical AFL during the ablation (p = 0.01) were independent predictors of symptomatic AFL during follow-up. The incidence of symptomatic AFL during follow-up was similar among patients who did and did not have long-term freedom from recurrent AF. CONCLUSIONS: In patients with AF who have either a history of AFL or an episode of typical AFL during an electrophysiologic study, symptomatic AFL is common after pulmonary vein isolation. Therefore, cavo-tricuspid isthmus ablation is appropriate during pulmonary vein isolation if AFL has been observed clinically or in the electrophysiology laboratory.

Atrial Fibrillation↗
PubMed2004

Catheter ablation of atrial flutter after orthotopic heart transplantation.

INTRODUCTION: Atrial arrhythmias, including atrial flutter, are common in orthotopic heart transplant recipients. However, only a small number of individual case reports describe the electrical circuit and catheter ablation of atrial flutter after heart transplantation. METHODS AND RESULTS: Detailed electrophysiologic evaluation and radiofrequency ablation of atrial flutter were performed in three patients after orthotopic heart transplantation. All cases involved a counterclockwise flutter circuit around the tricuspid annulus. All were successfully ablated at the isthmus between the tricuspid valve and the atrial anastomosis adjacent to the inferior vena cava. CONCLUSION: Atrial flutter involving a counterclockwise circuit around the tricuspid annulus is common in the heart transplant population. Based on the patients described in this study and other cases reported in the literature, this arrhythmia often is treated successfully by ablation of the isthmus between the tricuspid valve and the atrial anastomosis near the inferior vena cava.

Adult↗
PubMed1998

Nonpharmacologic Therapy of Atrial Fibrillation and Atrial Flutter.

The medical therapy of atrial fibrillation and atrial flutter is unsatisfactory for many patients since nonpharmacologic therapy is often necessary. Curative catheter ablation is the treatment of choice for atrial flutter. Primary success rates of 95% are routinely achieved in centers of excellence with relapse rates for atrial flutter of 5%-10%. Nonpharmacologic therapies in atrial fibrillation are more often palliative than curative. Catheter ablation of the AV junction with implantation of a permanent pacemaker is the primary nonpharmacologic therapy for medically refractory atrial fibrillation. The quality of life is improved by AV junction ablation, although survival is not. Curative therapy for atrial fibrillation is available with the surgical maze operation but that is primarily offered in conjunction with concomitant cardiac surgery. Recently a catheter ablative procedure to mimic the maze operation has had preliminary evaluation but remains investigational. A focal ablation procedure for paroxysmal atrial fibrillation has also entered into clinical trials.

Journal Article↗
PubMed1997

Atrial flutter: an uncommon pediatric manifestation of hyperthyroidism.

OBJECTIVE: Atrial flutter is an uncommon arrhythmia in the pediatric population except for the immediate newborn period or following atrial repair of congenital heart disease. In children the diagnosis of atrial flutter may be difficult, attributable to rapid atrioventricular conduction and superimposition of flutter waves on QRS and T waves. Atrial flutter secondary to hyperthyroidism has been rarely reported in older adults, but there are no reports of children presenting with atrial flutter as the initial manifestation of hyperthyroidism. CASE REPORT: We report an interesting case of hyperthyroidism in a 3-year-old presenting with congestive heart failure and atrial flutter with 1:1 atrioventricular conduction. The responses to adenosine administration and to cardioversion were unusual and ultimately helpful in suggesting the diagnosis of hyperthyroidism. CONCLUSION: When atrial flutter is encountered in a pediatric patient in whom there is 1:1 atrioventricular conduction, a lack of a response to adenosine, and persistent sinus tachycardia after cardioversion, the clinician should be alert to the possibility of thyrotoxicosis.

Adenosine↗
PubMed1999

Angiographic anatomy of the inferior right atrial isthmus in patients with and without history of common atrial flutter.

BACKGROUND: Although most ablative procedures undertaken for common atrial flutter target the inferior right atrial isthmus, comparative studies of the morphology of this area are lacking. Our study examines its angiographic anatomy, making correlations with postmortem specimens, to provide a better understanding of the anatomic substrate of this arrhythmia. METHODS AND RESULTS: The gross morphological features and dimensions of the area between the orifice of the inferior caval vein and the attachment of the septal leaflet of the tricuspid valve were determined from angiograms made in 23 patients with documented atrial flutter and 30 control subjects. For comparison, we studied 20 normal heart specimens. When viewed in right anterior oblique projection, 2 morphologically distinct areas were identified. In the specimens, the inferior isthmus measured a mean length of 30+/-4 mm, not significantly different from the dimensions obtained from angiograms of control subjects. The mean length of the isthmus, however, was greater in patients with common atrial flutter than those without (37+/-8 versus 28+/-6 mm). Patients with atrial flutter and structural heart disease had an even longer isthmus than those with flutter alone (39. 6+/-8 versus 33+/-7 mm). Compared with those without flutter, the atrial diameter was also larger in patients with flutter (57.6+/-9 versus 48.5+/-6 mm). Reevaluation carried out at follow-up 10+/-2 months after ablation did not show any reduction in atrial size, although contractility improved. CONCLUSIONS: The inferior isthmus and right atrium in patients with common atrial flutter were significantly larger than those in a control population.

Adult↗
PubMed1977

Idiopathic atrial flutter, high grade atrioventricular block and sino-atrial dysrhythmia in a young man. Effects of exercise testing.

A 25-year-old man with idopathic atrial flutter and high grade atrioventricular (AV) block is described. Postcardioversion, sino-atrial (SA) and AV nodal dysrhythmias occurred. Treadmill exercise during atrial flutter increased AV conduction to 2:1, and normalized SA and AV nodal function following cardioversion. A neurogenic basis for these arrhythmias is hypothesized.

Adult↗
PubMed2000

Predictors of success in radiofrequency catheter ablation of atrial flutter.

Radiofrequency catheter ablation of typical atrial flutter at the isthmus between the tricuspid annulus and the inferior vena cava is established. However in selected patients, the creation of a continuous linear lesion at the targeted isthmus requires a lengthened procedure or is not feasible at all and atrial flutter recurrences are common. In a retrospective analysis, we found that an intraoperatively determined distance between the tricuspid annulus and the inferior vena cava of <.2.5 cm is an independent predictor of a lengthened or failed ablation procedure. Additional equipment, e.g., long introducer sheaths, adapted ablation catheter design, or irrigated tip ablation, as well as alternative ablation approaches, e.g., linear lesions between the tricuspid annulus and Eustachian ridge, have been invented in order to increase the acute success rate or decrease fluoroscopy and procedure time. In a prospective study on the effects of various conduction properties at the isthmus between tricuspid annulus and inferior vena cava following radiofrequency ablation of atrial flutter, we showed previously that others than a complete bidirectional conduction block predicts a high recurrence rate of atrial flutter. For determination of transisthmal conduction properties following ablation, established mapping approaches are documentation of double potentials at the ablation line and right atrial activation sequence following posteroseptal and low lateral right atrial pacing. Novel threedimensional mapping systems, i.e., Carto(R) and EnSite(R), may further enhance the accuracy of conventional mapping techniques.

Atrial Flutter↗
PubMed2003

Long-term outcome of patients after successful radiofrequency ablation for typical atrial flutter.

The aim of the study was to determine the long-term freedom from atrial arrhythmias after radiofrequency ablation of atrial flutter and to determine the factors associated with recurrent arrhythmias. Radiofrequency ablation has emerged as the preferred treatment for recurrent, typical atrial flutter. Although the short-term results after radiofrequency ablation of atrial flutter have been widely reported, there is insufficient data on long-term outcome with respect to the occurrence of atrial arrhythmias in patients after successful ablation. The first 108 patients to undergo successful ablation for typical atrial flutter at the authors' institutions were followed prospectively until the occurrence of typical atrial flutter, atrial fibrillation, atypical atrial flutter, or death. Several prespecified clinical and procedural factors were tested using univariate and multivariate analysis as predictors of arrhythmia recurrence. Patients were followed for a minimum of 3 years and a maximum of 8 years, or until the first arrhythmia recurrence (average duration 17 +/- 17 months). Recurrences of typical atrial flutter were usually observed within the first 6 months (73%, n = 16), with the remainder (27%, n = 6) occurring between 6 months and 2 years, and none were observed later. Freedom from recurrence of typical atrial flutter was 80% at 1 year (95% CIs 72-89%), 73% at 2 years (CIs 63-83%), and 73% at 5 years (CIs 63-83%). By contrast, freedom from occurrence of atrial fibrillation or atypical atrial flutter progressively declined over time; 80% at 1 year (CIs 71-88%), 59% at 2 years (CIs 48-70%), and 33% at 5 years (CIs 19-48%). A history of atrial fibrillation or atypical atrial flutter prior to ablation was associated with an increased risk of occurrence during follow-up (relative risk 3.4, CIs 1.5-8.1, P < 0.05). Freedom from occurrence of any atrial arrhythmia was only 27% at 5 years (CIs 15-40%). After successful ablation of typical atrial flutter, recurrence of typical flutter is relatively uncommon and usually occurs early. However, there is a progressive occurrence of atrial fibrillation and/or atypical flutter during follow-up so that many patients require further antiarrhythmic or additional ablative therapy. Radiofrequency ablation of typical atrial flutter should be considered a palliative procedure for most patients and only one component of the long-term care of the patient with atrial tachyarrhythmias.

Aged↗
PubMed1997

Electrophysiologic characteristics and radiofrequency catheter ablation in patients with clockwise atrial flutter.

INTRODUCTION: Although the mechanism and radiofrequency catheter ablation of counterclockwise (typical) atrial flutter have been studied extensively, information about the electrocardiographic and electrophysiologic characteristics and effects of radiofrequency ablation in patients with clockwise atrial flutter is limited. METHODS AND RESULTS: Thirty consecutive patients with clinically documented paroxysmal clockwise atrial flutter were studied. Endocardial recordings and entrainment study using a "halo" catheter with 10 electrode pairs in the right atrium were performed. Radiofrequency energy was applied to the inferior vena cava-tricuspid annulus (IVC-TA) and/or coronary sinus ostium-tricuspid annulus (CSO-TA) isthmus to evaluate the effects of linear catheter ablation. Eighteen patients had both counterclockwise and clockwise atrial flutters, and 12 patients had only clockwise atrial flutter. Both forms of atrial flutter had similar flutter cycle lengths (232 +/- 30 vs 226 +/- 25 msec, P = 0.526) but reverse activation sequences. Right atrial pacing at a cycle length 20 msec shorter than the flutter cycle length from the CSO-TA isthmus, IVC-TA isthmus, and the area between the two isthmuses revealed concealed entrainment with stimulus-to-P wave intervals of 32 +/- 19, 95 +/- 14, and 50 +/- 17 msec (P = 0.022) in the counterclockwise form, and 110 +/- 12, 40 +/- 20, and 60 +/- 15 msec (P = 0.018) in the clockwise form. In clockwise atrial flutter, 20 patients with biphasic P waves in the inferior leads had the presumed exit site of slow conduction area located at the low posterolateral right atrium; 10 patients with positive P waves in the inferior leads had the presumed exit site located at the mid-high posterolateral right atrium. Among the 18 patients with both forms of atrial flutter, linear ablation lesions directed at the IVC-TA isthmus eliminated both forms of atrial flutter in 14 patients; in the remaining 4 patients, CSO-TA linear lesions eliminated the counterclockwise form and IVC-TA lesions eliminated the clockwise form. Among the 12 patients with the clockwise form only, CSO-TA linear lesions eliminated flutter in 2 and IVC-TA linear lesions eliminated flutter in 10 patients. Successful ablation was confirmed by creation of bidirectional conduction block in the IVC-TA and/or CSO-TA isthmus during pacing from the proximal coronary sinus and right posterolateral atrium sandwiching the linear lesions. During the follow-up period of 17 +/- 8 months, 2 patients had recurrence of clockwise atrial flutter, 1 patient had new onset of atypical atrial flutter, and 2 patients had new onset of atrial fibrillation. CONCLUSIONS: Counterclockwise and clockwise atrial flutters may have overlapping slow conduction areas with different exit sites. Radiofrequency catheter ablation using the linear method directed at the IVC-TA and CSO-TA isthmuses was feasible and effective in treating both forms of atrial flutter.

Adult↗
PubMed1989

Oral N-acetylprocainamide compared to quinidine plus digoxin in the chronic suppression of atrial flutter in humans.

Antiarrhythmic therapy for the suppression of atrial flutter has conventionally entailed the use of a class Ia agent such as quinidine or procainamide. However, atrial flutter often recurs despite the use of these conventional antiarrhythmic regimens. Experimental and clinical evidence suggests that the pharmacologic suppression of atrial flutter may depend on the prolongation of the atrial action potential duration and consequently the voltage-dependent refractoriness. Therefore, the efficacy and tolerance of the class III antiarrhythmic agent N-acetylprocainamide was compared to that of the conventional regimen of the class Ia agent quinidine combined with digoxin (to control ventricular response) in patients with a history of symptomatic sustained atrial flutter. The study was randomized but nonblinded, with a crossover to the alternate regimen if the first failed. Eighteen patients entered the study and were followed for up to 18 months. Of the 12 receiving N-acetylprocainamide (eight randomized and four crossovers), one (8%) failed therapy due to side effects, but none had atrial flutter. Of the 11 receiving quinidine and digoxin (10 randomized and one crossover), three (28%) had a recurrence of atrial flutter, two of whom also had intolerable side effects, and two more (18%) had side effects alone requiring withdrawal of therapy (total 46% failed). The probability of therapeutic success over time was greater (p less than 0.04) for N-acetylprocainamide than for quinidine and digoxin. The data suggest that N-acetylprocainamide may be more effective and better tolerated than the conventional regimen of quinidine plus digoxin. Therefore, large-scale blinded studies of the efficacy of N-acetylprocainamide in the suppression of atrial flutter may be warranted.

Acecainide↗