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Diagnosis and ablation of atrial flutter using a high resolution, noncontact mapping system.

The ablation of atrial flutter can sometimes be time consuming and unsuccessful using conventional catheter techniques especially in patients with recurrences after previous ablation procedures. Simultaneous high resolution mapping from multiple sites may overcome some of the limitations. Therefore, a new high resolution noncontact mapping system was used for diagnosis and ablation of atrial flutter in 15 patients. The mapping system consists of a catheter-mounted multielectrode array, an amplifier, and a computer workstation. Far-field potentials recorded by the multielectrode catheter are amplified, digitized, and sampled at 1.2 kHz, and digitally filtered to construct high resolution activation maps during tachycardia. Ablation catheters can be steered to target sites without fluoroscopy. In 12 of the 15 patients the analysis of the activation sequence during tachycardia showed a counter-clockwise, and in 1 of 15 patients a clockwise, rotating wavefront using the isthmus as part of the reentrant circuit. In two patients no tachycardia could be induced. In 3 of the 15 patients with previous conventional ablation procedures the gap in the line of block in the isthmus region was identified and marked on the animation model. The isthmus in the right atrium was ablated and isthmus block verified by the mapping system in all patients. No complications were observed. No recurrences of atrial flutter occurred during follow-up of 4 +/- 1.7 months. The total procedure and fluoroscopy time was 171 +/- 50.0 minutes and 24 +/- 12.7 minutes, respectively. In conclusion, the use of the new high resolution noncontact mapping system in patients with right atrial flutter is safe and highly effective. In patients with previously failed conventional ablation procedures the use of a noncontact mapping system may facilitate the identification of the gap in the line of block in the isthmus region and reablation of atrial flutter.

Adult↗

Electrophysiologic determinants of recurrent atrial flutter after successful termination by overdrive pacing.

The potential ability of electrophysiologic abnormalities to predict recurrence of atrial flutter was evaluated. Twenty-five patients with chronic atrial flutter resistant to combined digitalis and quinidine therapy were studied electrophysiologically after restoration of sinus rhythm by overdrive pacing or by eventual direct current cardioversion. Recurrence of atrial flutter was observed in 12 patients during a mean follow-up period of 17 months (range 3 to 50). Electrophysiologic testing included programmed high right atrial stimulation at a paced drive cycle length of 600 ms and incremental pacing up to 200-ms paced intervals. When coupling intervals of 90% of the drive cycle length were compared to coupling intervals of 48% of the drive cycle length, the increase in S1A1 interval, defined as the interval between the stimulus artifact and the atrial activation near the atrioventricular junction, was greater in patients with subsequent recurrence of atrial flutter (47 +/- 11 vs 21 +/- 18 ms). Stepwise logistic regression analysis identified the S1A1 increase to be the sole independent predictor of recurrence (p = 0.0082) while previous episodes of atrial flutter or the presence of organic heart disease were identified as dependent variables. Reclassification showed a 91% sensitivity and a 92% specificity. Correct classification was achieved in 92% of patients. The initiation of atrial dysrhythmia had no predictive value. The assessment of the S1A1 interval by programmed atrial stimulation appears helpful in delineating the patient risk of recurrent atrial flutter after termination by overdrive pacing.

Atrial Flutter↗

Conversion of atrial flutter to sinus rhythm by carotid sinus pressure.

Conversion of atrial flutter to normal sinus rhythm via carotid sinus stimulation by manual pressure is not a well-known phenomenon. Two cases of atrial flutter in which carotid sinus pressure restored the sinus rhythm are presented. Since this procedure is usually benign, it is recommended that it be tried on patients having atrial flutter with fast ventricular rate accompanied by hemodynamic decompensation. This may be particularly useful if the patient has been receiving digoxin, that is, when cardioversion may become potentially problematic. Electrophysiological mechanisms of conversion of atrial flutter to sinus rhythm are discussed.

Aged↗

Conduction properties of the crista terminalis in patients with typical atrial flutter: basis for a line of block in the reentrant circuit.

INTRODUCTION: Previous mapping studies in patients with typical atrial flutter have demonstrated the crista terminalis to be a posterior barrier of the reentrant circuit forming a line of block. However, the functional role of the crista terminalis in patients with or without a history of atrial flutter is not well known. The aim of this study was to determine whether the conduction properties of the crista terminalis are different between patients with and those without a history of atrial flutter. METHODS AND RESULTS: The study population consisted of 12 patients with clinically documented atrial flutter (group 1) and 12 patients with paroxysmal supraventricular tachycardia as well as induced atrial flutter (group 2). A 7-French, 20-pole, deflectable Halo catheter was positioned around the tricuspid annulus. A 7-French, 20-pole Crista catheter was placed along the crista terminalis identified by the recording of double potentials with opposite activation sequences during typical atrial flutter. After sinus rhythm was restored, pacing from the low posterior right atrium near the crista terminalis was performed at multiple cycle length to 2:1 atrial capture. No double potentials were recorded along the crista terminalis during sinus rhythm in both groups. In group 1, the longest pacing cycle length that resulted in a line of block with double potentials along the crista terminalis was 638 +/- 119 msec. After infusion of propranolol, it was prolonged to 832 +/- 93 msec without change of the interdeflection intervals of double potentials. In group 2, the longest pacing cycle length that resulted in a line of block with double potentials along the crista terminalis was 214 +/- 23 msec. After infusion of procainamide, it was prolonged to 306 +/- 36 msec with increase of interdeflection interval of double potentials. CONCLUSION: The crista terminalis forms a line of transverse conduction block during typical atrial flutter. Poor transverse conduction property in the crista terminalis may be the requisite substrate for clinical occurrence of typical atrial flutter.

Adult↗

Determinants of recurrent atrial flutter after cardioversion.

Eighteen male patients (mean age 59 years) who were electrically cardioverted for pure atrial flutter were retrospectively studied to determine those factors influencing the maintenance of regular sinus rhythm or reversion to atrial flutter. Six months after successful cardioversion, 10 patients (55%) had recurrent atrial flutter and eight patients (45%) were still in sinus rhythm. The two groups were not significantly different with respect to age, symptomatology, abnormalities on the 12 lead electrocardiogram (during sinus rhythm), or the administration of digoxin and a class Ia antiarrhythmic agent (after cardioversion). There was a trend for those patients with recurrent atrial flutter to have a higher incidence of underlying heart disease and previous episodes of atrial flutter than the non-recurrent group. There were statistically significant differences between the recurrent and non-recurrent groups with respect to echocardiographically determined left atrial size and left ventricular ejection fraction. Patients with a left atrial size greater than 45 mm or with an ejection fraction less than 45% were all at high risk for recurrent atrial flutter after successful cardioversion.

Aged↗

Transesophageal atrial pacing using a pill electrode for the termination of atrial flutter.

To determine the efficacy of transesophageal rapid atrial pacing with a "pill-electrode" for the termination of atrial flutter, we studied 14 consecutive unselected patients presenting with atrial flutter of various etiologies. The bipolar pill-electrode (interelectrode distance 13 mm) was introduced orally without sedation. Of 14 pacing attempts, atrial capture was obtained in 13 (93 percent), and sustained alteration in rhythm (atrial fibrillation, sinus rhythm or type 2 flutter) in 12 (86 percent). Normal sinus rhythm occurred in six (43 percent), in all of whom it was preceded by transient atrial fibrillation. There was no difference in baseline flutter rates, pacing rates for atrial capture, or duration of flutter between patients reverting to sinus rhythm and those remaining in flutter or converting to atrial fibrillation. Pacing was well tolerated in all but one subject. Thus, esophageal pacing with the pill-electrode was simple to perform, well-tolerated and highly successful for atrial capture in patients with atrial flutter. Although it had a lower success rate than DC cardioversion in producing sinus rhythm, the simplicity of application makes it a useful initial alternative, particularly in patients in whom cardioversion may be hazardous.

Adult↗

Identification and ablation of atypical atrial flutter. Entrainment pacing combined with electroanatomic mapping.

Differentiation between typical and atypical atrial flutter solely based upon surface ECG pattern may be limited. However, successful ablation of atrial flutter depends on the exact identification of the responsible re-entrant circuit and its critical isthmus. Between August 2001 and June 2003, we performed conventional entrainment pacing within the cavotricuspid isthmus in 71 patients with sustained atrial flutter. In patients with positive entrainment we considered the arrhythmia as typical flutter and treated them with conventional ablation of the cavotricuspid isthmus. As a consequence of negative entrainment we performed 3D-electroanatomic activation mapping (CARTO trade mark ). Conventional ablation of the right atrial isthmus was successful in all patients (n = 54) with positive entrainment. We performed electroanatomic mapping in the remaining 17 patients (14 male; age 60.9 +/- 16 years) resulting in the identification of 6 cases with typical and 11 cases with atypical flutter. Therefore, entrainment pacing was able to predict the true presence of typical atrial flutter in 91.5%. Atypical flutter was right sided in 4 patients and left sided in 7 cases. Electrically silent ("low voltage") areas probably demonstrating atrial myopathy were identified in all cases with left sided and in 2 patients with right sided flutter. In these patients targets for ablation lines were located between silent areas and anatomic barriers (inferior pulmonary veins, mitral respectively tricuspid annulus, or vena cava inferior). In 1 patient, the investigation was stopped due to variable ECG pattern and atrial cycle lengths. In the remaining cases, ablation was acutely successful. One patient, after surgical closure of a ventricular septal defect, demonstrated a dual-loop intra-atrial reentry tachycardia dependent on two different isthmuses. This arrhythmia required ablation of those distinct isthmuses to be interrupted. After a mean follow-up of 8.8 +/- 3.4 months, there was one patient with a recurrence of left-sided atrial flutter. Another patient developed permanent atrial fibrillation shortly after the procedure. Mean duration time of the procedure was 235.6 +/- 56.4 min (right atrium: 196 +/- 17.3 min; left atrium: 267.2 +/- 59.5 min), and average fluoroscopy time was 21.8 +/- 11.7 min (right atrium: 9.5 +/- 6 min; left atrium: 28.9 +/- 7 min). There was no incidence of serious complications associated with these procedures. In conclusion, conventional pacing in the cavotricuspid isthmus combined with electroanatomic mapping was an effective method to differentiate between typical and atypical atrial flutter. Electroanatomic mapping was a powerful tool both for identification of different atrial re-entrant circuits including their critical isthmuses as well as for effective application of individual ablation line strategies.

Adolescent↗

The influence of exercise on atrial flutter.

To study the effect of exercise on atrial flutter the electrocardiogram was recorded continuously before, during and after low level treadmill walking in twenty-two ambulatory patients. Atrial flutter rates increased during exercise testing in four patients. Improved A-V conduction with consequent higher ventricular rates occurred during exercise in thirteen subjects. One patient, with 4:1 conduction at rest, continued with 4:1 block throughout exercise testing, was believed to be over-digitalized. During the recovery period after exercise, ten patients transiently developed periods of Wenckebach A-V block. Walking exercise induced 1:1 conduction in six patients and was promoted by the following circumstances: 1) atrial rates of 250/min or less; 2) inadequate dosage of digitalis; and 3) the administration of quinidine. For the patient with chronic atrial flutter, treadmill testing provides a simple method for demonstrating the range of changes of A-V conduction and for deriving implications for appropriate drug therapy.

Adult↗

Thromboembolism in chronic atrial flutter: is the risk underestimated?

OBJECTIVES: We sought to evaluate the risk of thromboembolic events in the presence of chronic atrial flutter and to determine the impact of anticoagulation therapy, if any, on this risk. BACKGROUND: Thromboembolic events are thought to be rare after cardioversion of atrial flutter. METHODS: This study was a retrospective analysis of 110 consecutive patients referred to the electrophysiology laboratory for cardioversion of chronic atrial flutter from 1986 to 1996. Atrial flutter was present for at least 6 months. Of the 110 patients reviewed, 100 had adequate information available regarding the effectiveness of anticoagulation (mean age 64 years, range 27 to 86; 75 men, 25 women; mean left ventricular ejection fraction 42%). RESULTS: Thirteen patients (13%) had a thromboembolic event. Of these, seven were attributable to causes other than atrial flutter. In the remaining six patients (6%), thromboembolic events occurred during a rhythm of atrial flutter or after cardioversion to sinus rhythm. Other causes of thromboembolism were excluded. Effective anticoagulation was associated with a decreased risk of thromboembolism (p = 0.026). CONCLUSIONS: Patients with chronic atrial flutter are at an increased risk of thromboembolic events. Effective anticoagulation may decrease this risk.

Adult↗

Relationship between polarity of the flutter wave in the surface ECG and endocardial atrial activation sequence in patients with typical counterclockwise and clockwise atrial flutter.

BACKGROUND: The relation between ECG and activation patterns within atria in typical atrial flutter (AFL) patients (pts) has not been defined due to the lack of simultaneous multisite right and left atrial mapping. METHODS: In 13 pts with AFL, a Halo catheter was positioned along tricuspid annulus and multipolar catheters were placed in right atrial appendage, His bundle region, coronary sinus (CS), proximal portion of right pulmonary artery (Bachmann's bundle region, BB) and esophagus (Eso) to record right and left atrial activation simultaneously. RESULTS: In counterclockwise (CCW) AFL (11 pts), 9 showed negative flutter wave (F) and 2 positive F in the inferior leads. CCW/negative F; CS electrograms (EGs) were proximal to distal, Eso EGs were inferior to superior and BB activation was later than CS and Eso. positive F; BB activation was earlier than CS. Eso EGs were superior to inferior or simultaneous. In clockwise (CW) AFL (7 pts), 5 showed positive F and 2 negative F. CW/positive F; BB activation preceded Eso and CS. Eso EGs were superior to inferior. CS EGs were proximal to distal (1), middle to proximal, distal (3) or proximal, distal to middle (1). negative F; CS EGs were proximal to distal. CS activation was earlier than BB or CS and BB activation were simultaneous. Eso EGs were inferior to superior. CONCLUSION: Impulse conduction to the left atrial free wall through either lower or upper interatrial connection is a major determinant of ECG morphology in AFL.

Adult↗

[Analysis of the structure of cardiac rhythm in atrial flutter].

Heart rhythm was studied by computer in 67 patients with atrial flutter of different etiology. It was discovered that respiratory activity has an influence on the conduction of atrial flutter waves to the ventricles. In the majority of cases, the conduction of atrial waves to the ventricles is multiple with a constant conduction ratio. However, in some cases the conduction of atrial flutter waves via the atrioventricular system occurs according to the Samoilov-Wenckebach periodicals. In the latter case and in atrial flutter with a conduction ratio of 4:1, one-third of patients manifest, after the recovery of the sinus rhythm, atrioventricular blockade, grade 1.

Adult↗

Three-dimensional noncontact mapping defines two zones of slow conduction in the circuit of typical atrial flutter.

The cavotricuspid isthmus (CTI) is a slow conduction area in the circuit of typical atrial flutter. However, conventional methods are limited by the inaccuracy of measurements of distance on the surface of the heart. The aim of the study was to define the conduction properties of the atrial flutter circuit along the tricuspid annulus by using a three-dimensional noncontact mapping system. In 34 atrial flutter patients (30 men, 4 women; mean age 54 +/- 14; 27 counter-clockwise, 4 clockwise, and 3 both), a noncontact multielectrode array was used to reconstruct electrograms in the right atrium. Isochronal and isopotential propagation mapping was performed during atrial flutter. The conduction velocity was calculated by dividing conduction time by surface distance. The right atrium along the tricuspid annulus was divided into five regions: lateral wall, superior right atrium, septum, septal CTI, and lateral CTI. Conduction velocities were 0.99 +/- 0.85, 1.67 +/- 1.21, 1.58 +/- 1.05, 0.82 +/- 0.72, and 1.68 +/- 1.00 m/s in counter-clockwise and 0.81 +/- 0.71, 2.61 +/- 1.90, 1.52 +/- 0.91, 0.91 +/- 0.80 and 1.91 +/- 0.83 m/s in clockwise, respectively. Conduction velocities were significantly slower in the septal CTI and lateral wall than in the lateral CTI, the septum, and the superior right atrium (P < 0.05). No significant difference was found between the septal CTI and the lateral wall. Conduction within the septal CTI was slower in patients treated with antiarrhythmic agents than in untreated patients (P < 0.05). The septal part of the CTI (but not the lateral CTI) and the lateral wall are slow conduction zones in the atrial flutter circuit, and both may, therefore, be mechanically important for the development of atrial flutter.

Atrial Flutter↗

Radiofrequency catheter ablation of common atrial flutter in 200 patients.

INTRODUCTION: The purpose of this study was to evaluate the efficacy and safety of radiofrequency (RF) catheter ablation of common atrial flutter and to determine the optimum target sites in a large series of patients. Three different approaches were used to target the ablation site. The first used a combined anatomic and electrophysiologic approach, whereas the second and the third approaches relied primarily on anatomic guidelines to target the critical area in the atrial flutter reentrant circuit located in the low right atrium. BACKGROUND: Recent studies report the efficacy of RF current application in the low right atrial region to interrupt and prevent recurrences of common atrial flutter using either anatomic or electrophysiologic targets. However, larger groups of patients are required to confirm the efficacy of this technique and to specify the target sites. METHODS AND RESULTS: Two hundred consecutive patients with drug-resistant common atrial flutter were studied. In the first 50 patients, target sites were localized using both anatomic landmarks and electrophysiologic parameters. The anatomic landmarks were area 1 between the tricuspid valve and inferior vena cava orifice; area 2 between the tricuspid valve and coronary sinus ostium; and area 3 between the inferior vena and coronary sinus. The electrophysiologic criterion was to ablate when there was an atrial electrogram occurring during the plateau phase (preceding F wave). The first targeted area was that giving the more stable catheter position. In the following 30 patients, we assessed the effect of RF energy application in a single line to area 1 in the first 10 patients, area 2 in the next 10, and area 3 in the last 10 patients. In the last 120 patients, RF energy was applied only in area 1 using repeated applications. RF energy of 12 to 30 W, or that achieving a temperature of 70 degrees C, was applied for 60 to 90 seconds at each site. The endpoint of the ablation procedure was interruption and noninducibility of common atrial flutter in the first 110 patients and additional isthmal block in 48 of the last 90 patients. Overall, atrial flutter was interrupted and rendered noninducible after a single session in 191 (95%) patients and could not be interrupted in 9 (4.5%) patients. The mean number of RF applications was 12 +/- 8. After a mean follow-up of 24 +/- 9 months, recurrences occurred in 31 (15.5%) patients, 26 of whom underwent a successful second or third session without further recurrences of atrial flutter. Atrial fibrillation not documented before the ablation was detected in 11 patients. On a retrospective analysis of the final successful site in the first group of 50 patients, the location was in area 1 in 39% of patients; area 2 in 36% of patients, and area 3 in 25% of patients. Atrial electrograms recorded at these sites showed a single spike pattern in 46% of patients, and double spike pattern (28%) or fractioned electrogram in 26% patients. When lines of RF lesions were placed at several sites, they produced a success rate of 70%, 40%, and 10% at areas 1, 2, and 3 respectively. In the last series of 120 patients, the procedure was successful in 119 patients: 92% of whom were successfully treated only by a linear lesion between the tricuspid annulus isthmus and the inferior vena cava, and the other 8% by additional applications near the coronary sinus ostium. No complications were observed. CONCLUSIONS: RF catheter ablation of atrial flutter can be done with a high success rate and is safe. The highest success rate is achieved with RF energy applied in the isthmus between the inferior vena cava orifice and the tricuspid valve. However, 15.5% of patients need multiple sessions to achieve success because of recurrence of flutter. Further follow-up is needed to evaluate the long-term effects of this procedure.

Adult↗

Electropharmacologic effects of class I and class III antiarrhythmia drugs on typical atrial flutter: insights into the mechanism of termination.

BACKGROUND: Acute effects of class I and class III antiarrhythmia drugs on the reentrant circuit of typical atrial flutter are not fully studied. Furthermore, the critical electrophysiologic determinants of flutter termination by antiarrhythmia drugs are not clear. METHODS AND RESULTS: The study population consisted of 36 patients (mean age, 53+/-17 years) with clinically documented typical atrial flutter. A 20-pole "halo" catheter was positioned around the tricuspid annulus. Incremental pacing was performed to measure the conduction velocity along the isthmus and lateral wall, and extrastimulation was performed to evaluate atrial refractory period in the baseline state and after intravenous infusion of ibutilide, propafenone, and amiodarone. Efficacy of these drugs in conversion of typical atrial flutter and patterns of termination were also determined. Ibutilide significantly increased the atrial refractory period and decreased conduction velocity in the isthmus at short pacing cycle length. It terminated atrial flutter in 8 (67%) of 12 patients after prolongation of flutter cycle length due to increase (86+/-19%) of conduction time in the isthmus. Propafenone predominantly decreased conduction velocity with use dependency and significantly increased atrial refractory period, but it only converted atrial flutter in 4 (33%) of 12 patients. Amiodarone had fewer effects on atrial refractory period and conduction velocity than did ibutilide and propafenone, and it terminated atrial flutter in only 4 (33%) of 12 patients. Termination of typical atrial flutter was due to failure of wave front propagation through the isthmus, which occurred with cycle length oscillation, abruptly without variability of cycle length, or after premature activation of the reentrant circuit. CONCLUSIONS: Ibutilide, with a unique increase in atrial refractoriness, was more effective in conversion of atrial flutter than were propafenone and amiodarone.

Adult↗

Radiofrequency catheter ablation of atrial flutter after orthotopic heart transplantation.

INTRODUCTION: Antiarrhythmic drug refractory recurrent atrial flutter occurred in a 39-year-old man who had undergone successful orthotopic heart transplantation 3 months ago. METHODS AND RESULTS: At electrophysiologic study, the transplanted right atrium showed type I atrial flutter. The recipient right atrium was in sinus rhythm with complete atrioatrial dissociation of electrical activity. Mapping demonstrated double-spike electrograms in the low posterior region of the donor right atrium. During radiofrequency current application near this site, the double potentials were dissociated progressively and atrial flutter was terminated immediately. Thereafter, both the recipient and the transplanted atria were in sinus rhythm of different cycle lengths with continued electrical dissociation. CONCLUSION: This is the first report of successful radiofrequency catheter ablation of atrial flutter in a transplanted heart. Although mapping of the arrhythmia is more difficult due to the large circumference of the right atrium, which consists of parts of the recipient right atrium and the transplanted atrium, ablation should be considered in those patients with drug refractory supraventricular tachyarrhythmias.

Adult↗

Characterization of the excitable gap in human type I atrial flutter.

OBJECTIVES: We sought to characterize the excitable gap of the reentrant circuit in atrial flutter. BACKGROUND: The electrophysiologic substrate of typical atrial flutter has not been well characterized. Specifically, it is not known whether the properties of the tricuspid valve isthmus differ from those of the remainder of the circuit. METHODS: Resetting was performed from two sites within the circuit: proximal (site A) and distal (site B) to the isthmus in 14 patients with type I atrial flutter. Resetting response patterns and the location where interval-dependent conduction slowing occurred were assessed. RESULTS: Some duration of a flat resetting response (mean +/- SD 40.1 +/- 20.9 ms, 16 +/- 8% of the cycle length) was observed in 13 of 14 patients; 1 patient had a purely increasing response. During the increasing portion of the resetting curve, interval-dependent conduction delay most commonly occurred in the isthmus. In most cases, the resetting response was similar at both sites. In three patients, the resetting response differed significantly between the two sites; this finding suggests that paced beats may transiently change conduction within the circuit or the circuit path, or both. CONCLUSIONS: Some duration of a flat resetting response was observed in most cases of type I atrial flutter, signifying a fully excitable gap in all portions of the circuit. The isthmus represents the portion of the circuit most vulnerable to interval-dependent conduction delay at short coupling intervals.

Action Potentials↗

Splitting of high right atrial potentials in atrial flutter with rapid pacing.

Rapid pacing from the high right atrium was performed in 7 patients with atrial flutter in whom potentials with multicomponent high-frequency deflections were recorded at the high right atrium to examine the origin of these potentials during transient entrainment in atrial flutter. In all of the patients with relatively slow rapid pacing, the potentials were captured orthodromically through the atrial flutter reentry circuit with a long conduction time. With more rapid pacing, the potentials were split into 2 associated components: P1 and P2. P1 was captured antidromically with a short conduction time whereas P2 was captured persistently in an orthodromic direction through the reentry circuit with a progressively long conduction time. In 3 of the 7 patients, atrial flutter was converted into another atrial flutter by rapid pacing. During this other atrial flutter, the potentials at the high right atrium were split from the beginning to form double potentials: D1 and D2. During rapid pacing, D1 and D2 were fused, and D1 was captured antidromically whereas D2 was captured orthodromically through the reentry circuit. In sinus rhythm, the potentials at the high right atrium formed fractionated potentials. These findings suggest that 1) fractionated potentials may represent 2 atrial regions with different conductivity properties, 2) fractionated potentials may be able to change into double potentials, and 3) double potentials may be attributable to their conductivity properties rather than refractoriness.

Action Potentials↗

Restoring Sinus Rhythm in Patients With Atrial Flutter and Fibrillation: Pharmacologic or Electrical Cardioversion?

Atrial fibrillation and atrial flutter, the most frequently encountered tachyarrhythmias requiring treatment, have become a major focus for clinical and basic research in recent years. Restoration and maintenance of sinus rhythmn, having been shown to improve exercise capacity, alleviate symptoms, and reduce the incidence of thromboembolic events, may be the optimal management strategy. Identification of the safest, most efficacious and cost-effective means of restoring sinus rhythm is necessary prior to the institution of optimal antiarrhythmic therapy to maintain sinus rhythm. Potential advantages of pharmacologic compared with electrical cardioversion include lack of need for general anesthesia and likely lower cost. Pharmacologic conversion include lack of need for general anesthesia and likely lower cost. Pharmacologic conversion has been accomplished with drugs that prolong atrial refractorinerss, including class Ia (quinidine, procainamide, disopyramide), class Ic (flecainide, propafenone), and class II (sotalol, amiodarone) compounds. The so-called pure class III agents were created to overcome the blocker side effects of sotalol and the complex pharmacodynamic profile of amiodarone. Two such agents are dofetilide, which selectively blocks the rapid component of the delayed rectifier current (Ikr) and ibutilide, which augments the slow inward sodium current, with a smaller component of action mediated by the block of Ikr. Reported overall conversion rates for recent onset atrial fibrillation and atrial flutter were 31% and 54% for difetilide, respectively, and 29-31% and 38-63%, respectively, for ibutilide. Proarrhythmia, manifested as polymorphic ventricular tachycardia requiring cardioversion, was a significant early side effect of both agents. Data from clinical trtials with these new agents, combined with increasing nowledge of the electrophysiologic substrate for these arrhythmias, has renewed initerest in the development of safer, more efficacious class IIIdrugs for atrial fibrillation and atrial flutter conversion.

Journal Article↗